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Журнал «Практическая онкология» Том 6, №1, 2023

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Вплив куркуміну та кверцетину на патогенез раку молочної залози шляхом зниження регуляції miR-632 та miR-137

Вплив куркуміну та кверцетину на патогенез раку молочної залози шляхом зниження регуляції miR-632 та miR-137

Авторы: Elgin Türköz Uluer, Muhammet Yusuf Pekmezci, Hilal Kabadayi Ensarioğlu, Mahmut Kemal Özbilgin
Manisa Celal Bayar University, Manisa, Turkey

Рубрики: Онкология

Разделы: Клинические исследования

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Резюме

Актуальність. Куркумін і кверцетин виявилися дуже ефективними проти раку молочної залози. Однак повністю їх протипухлинні механізми невідомі. У цьому дослідженні вивчено вплив куркуміну та кверцетину на ріст лінії клітин раку молочної залози людини MCF-7 та MDA-MB-231 шляхом регуляції miR-632 та miR-137. Матеріали та методи. Клітини MCF-7 і MDA-MB-231 обробляли куркуміном і кверцетином у різних розведеннях протягом 24 і 48 годин. Життє­здатність клітин оцінювали за допомогою MTT-аналізу. Кількісна полімеразна ланцюгова реакція в реальному часі була використана для виявлення експресії miR-632 і miR-137 у клітинах MCF-7 і MDA-MB-231, оброблених куркуміном і кверцетином. Результати. Наші результати показали, що ­50-мкМ розведення куркуміну та кверцетину протягом 24 годин було більш ефективним щодо пригнічення росту клітин MCF-7 та MDA-MB-231. У групах, які отримували куркумін і кверцетин, експресія miR-137 і miR-632 була знижена порівняно з конт­рольними групами. Експресія miR-137 у клітинній лінії ­MCF-7 була нижчою, ніж у клітинній лінії MDA-MB-231. Висновки. Використання куркуміну і кверцетину зменшувало ріст лінії клітин раку молочної залози людини MCF-7 і MDA-MB-231 шляхом зниження регуляції miR-137 і miR-632. Цей висновок показав, що куркумін і кверцетин можуть бути використані як терапевтичний засіб, а також що miR-137 і ­miR-632 застосовуються для діагностики, оцінки ефективності лікування та прогнозу при раку молочної залози.

Background. Curcumin and quercetin have been found to be very effective against breast cancer. However, their anticancer mechanisms of are not known completely. This study investigated the curcumin and quercetin effects on growth of MCF-7 and MDA-MB-231 human cancer breast cell line through regulation of miR-632 and miR-137. Materials and methods. MCF-7 and MDA-MB-231 cells were treated with curcumin and quercetin at various dilutions for 24 and 48 hours. Cell viability was assessed using MTT assay. Quantitative real-time polymerase chain reaction was used to detect the expression of miR-632 and miR-137 in curcumin- and quercetin-treated MCF-7 and MDA-MB-231 cells. Results. Our results showed that 50 μM dilution of curcumin and quercetin for 24 hours was more effective in inhibiting MCF-7 and MDA-MB-231 cells growth. In curcumin- and quercetin-treated groups, miR-632 and miR-137 expression was downregulated compared to control groups. The expression of miR-137 in MCF-7 cell line was lower than in MDA-MB-231 cell line. Conclusions. Curcumin and quercetin treatment decreased the growth of MCF-7 and MDA-MB-231 human cancer breast cell line by downregulating miR-137 and miR-632. This finding indicated that curcumin and quercetin may be used as a therapeutic agent, and also that miR-137 and miR-632 are used for the diagnosis, evaluation of treatment efficacy and prognosis in breast cancer.


Ключевые слова

куркумін; кверцетин; MCF-7; ­MDA-MB-231; miR-137; miR-632

curcumin; quercetin; MCF-7; MDA-MB-231; miR-137; miR-632

doi: http://dx.doi.org/10.22141/2663-3272.6.1.2023.78

Introduction

Breast cancer (BC) is the most commonly diagnosed cancer (24.5 % of total cases) and the leading cause of cancer death (15.5 %) among women, worldwide in 2020 [1]. In the treatment of BC, surgery, radiotherapy, chemotherapy, hormonal therapy, targeted therapy, or a combination of these can be used [2, 3]. Especially in advanced and metastatic breast cancers, tumor heterogeneity and side effects of drugs, and resistance to drugs limit treatment possibilities. It was suggested that the microRNAs (miRNA) regulate the most common molecular mechanism in tumor pathogenesis, and can be used as diagnostic or prognostic marker, and therapeutic targets in breast cancer [4].
Quercetin, is a plant flavonoid found in fresh fruits, vegetables, leaves, and seeds [5, 6]. Quercetin is an antioxidant and free radical scavenger [7], an inhibitor of iNOS synthase [8] and xanthine oxidase [9, 10], and modulator of gene expression [11, 12]. Studies have shown that quercetin can be used in diseases such as coronary heart disease [13], diabetes [14], and cancers [15, 16]. Quercetin also has anti-cancer effects that inhibit the growth, proliferation, and progression of cancer cells. It shows these effects via phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), Wnt/β-catenin, Janus kinase (JAK)/signal transducer and transcription activator (STAT), mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NFκB) and p53 signaling pathway [17]. In addition, quercetin also can change the activity of oncogenic and tumor suppressor miRNAs and lncRNAs [5, 18–20].
Curcumin is the active compound of the Curcuma longa rhizome, a member of the ginger family (Zingiberaceae) [2, 21, 22]. It has been shown that curcumin inhibits cell proliferation, migration, invasion, angiogenesis, and inflammation, induces apoptosis, and cell cycle arrest, and increases the sensitivity of tumor cells to chemotherapy and radiotherapy in different types of cancers including breast cancer [22–24]. It has also been shown in previous studies that curcumin affects signaling pathways such as PI3K-Akt-mTOR, MAPK, JAK-STAT, NF-kB, Wnt/β-catenin which plays a role in the development and progression of breast cancer, and molecules that affect apoptosis and cell cycle through the regulation of specific miRNAs [2, 22, 25–28].
Micro-RNAs (miRNAs) are short endogenous RNAs that can repress target gene expression and regulate various human diseases including cancers [29, 30]. In addition, targeting miRNA may be a biomarker for early diagnosis and prognosis for many diseases and used as a novel therapeutic strategy for the treatment of cancer such as breast cancer [22, 30–38]. Furthermore, many signaling pathways and epigenetically dysregulated DNAs and miRNAs can be affected by curcumin and quercetin [5, 22].
MiR-632 is involved in tumorigenesis and its overexpression has been implicated in many cancers such as breast cancer, gastric cancer, laryngeal squamous cell carcinoma, and hepatocellular carcinoma [30, 39–41]. It was reported that miR‐632 expression was found higher in invasive and metastatic breast cancer cells than in mammary epithelial cells [30]. On the other hand, miR-137 has been shown in studies to act as a tumor suppressor in many cancer types [42–44]. Upregulation of miR-137 expression has also been shown to reduce cell proliferation, migration, and metastasis, and stimulate cell cycle arrest, differentiation, and apoptosis [42–44]. All these features show miR-137 and miR-632 as targets for diagnosis, treatment, and prognosis in many cancer types [30, 42, 45, 46].
In this study, we aimed to investigate the effects of curcumin and quercetin on MCF-7 and MDA-MB-231 breast cancer cell lines via miR-632 and miR-137.

Materials and methods

MCF-7 (ACC115, DSMZ, Braunschweig, Germany) and MDA-MB-231 (92020424, ECACC, Salisbury, UK) breast cancer cells were used in this study. Both MCF-7 and MDA-MB-231 cells were cultured with 10% FBS (FBS, S0113, Biochrom AG, Berlin, Germany), 1% penicillin-streptomycin (Capricorn Scientific, Ebsdorfergrund, Germany) and 1% L-glutamine (Capricorn Scientific, Ebsdorfergrund, Germany) included RPMI 1640 (F1213, Biochrom AG, Berlin, Germany). Cells were maintained in a humidified atmosphere at 37 °C and 5% CO2 and subcultured when they reached 70–80% confluency.
Cell viability assay
MCF-7 and MDA-MB-231 cells were seeded in 96 well culture dishes at a density of 5 × 103/mL cells in each well with 100 µL of the medium. The cells were incubated for 24 hours. The next day, curcumin (C1386, Sigma-Aldrich, Darmstadt, Germany) and quercetin (Q4951, Sigma-Aldrich, Darmstadt, Germany) were dissolved with dimethyl sulfoxide (DMSO, Fisher Scientific, New Hampshire, USA) media to 100 μM. It was further diluted in a culture medium then 50, 25, 12.5, and 5 μM were applied to the cells. The MCF-7 and MDA-MB-231 cells were incubated with different concentrations of curcumin and quercetin for 24 and 48 h. Cell viability was estimated by MTT (2,5-diphenyl-2H-tetrazolium bromide) assay. MTT solution (Glentham life sciences, GC4568) was prepared in 5 mg/mL of phosphate-buffered saline (PBS) just before use and was filtered. After the treatment procedure, 10 μl MTT solution and 90 μl culture medium were added to each well and incubated for 4 h at 37 °C. The process was stopped by adding 50 μl DMSO to each well. Absorbance at 540 nm (Abs540) was measured with a microplate reader (BioTek Instruments Inc, ELX800UV, USA), using Abs540 as the reference wavelength.
Cultivation of cells with сurcumin and quercetin
Cells were divided into six groups. The first group was MCF-7 control group which was cultured with standard culture medium, the second group was MCF-7 cells trea–ted with 50 μM curcumin and the third group was MCF-7 cells treated with 50 μM quercetin for 24 hours. The fourth group was the MDA-MB-231 control group WHICH was cultured with standard culture medium and the fifth group was formed with the application of 50 μM curcumin and the sixth group was 50 μM quercetin treated for 24 hours.
Quantitative real-time PCR (qRT-PCR)
Cells were suspended using TRIzolTM (Thermo Fisher) reagent and total RNA was extracted using Hybrid-R miRNA kit (GeneALL-325-150) purification kit following manufacturer’s instructions. Isolated RNA’s quality and concentration were detected using nanodrop. Assessed RNA purity (260/280) ranged between 1.8 and 2.
The reverse transcription of complementary DNA (cDNA) synthesis was performed with 2 μg total RNA using the WizScript™ cDNA Synthesis Kit (High Capacity) for 120 min at 37 °C followed by 10 min at 85 °C. For miRNAs specific stem-loop RT primers were used.
The miRNA-specific RT primers were synthesized as shown (Table 1).
Gene expression analysis was performed on Roche LC480 using 2x WizPure™ qPCR Master (SYBR) following the manufacturer’s instructions. The PCR cycling conditions included an initial denaturation at 95 °C for 10 min followed by 40 cycles of denaturation at 95 °C for 15 se–conds, annealing at 60 °C for 15 seconds, and extension at 72 °C for 60 seconds. The oligonucleotide-specific primers were synthesized as shown (Table 2).
The housekeeping gene for miRNAs was U6. Relative fold changes in gene expression were calculated based on the 2−ΔΔCT comparative method (Livak and Schmittgen 2001; Schmittgen and Livak 2008).

Statistical analysis

Statistical analysis was done with GraphPad Prism 8.0. Multiple comparisons were performed using a one-way ANOVA test followed by Sidak’s correction. The value of P < 0.05 was considered significant.

Results

Cell viability and cytotoxicity
MCF-7 and MDA-MB-231 cells were treated with curcumin and quercetin at various dilutions for 24 and 48 h. Cell viability was determined as described above by the MTT assay. Curcumin and quercetin inhibited the growth of MCF-7 and MDA-MB-231 cells in a dose and time-dependent manner. Our results showed that 50-μM dilution of curcumin and quercetin for 24 hours was more effective in inhibiting MCF-7 and MDA-MB-231 cell growth when compared with other dilutions.
Quantitative real-time PCR
In curcumin and quercetin-treated groups miR-137 expression was down-regulated compared to control groups. When we compared the curcumin and quercetin-administered groups within themselves, it was determined that the expression of miR-137 in the MCF-7 cell line was lower than MDA-MB-231 cell line (Table 3, Fig. 1).
When the expression of miR-632 was examined, it was observed that miR-632 expression was down-regulated in breast cancer cell lines treated with curcumin and quercetin compared to the untreated control group. When we compared the curcumin and quercetin-treated groups with each other miR-632 expressions were higher in the MCF-7 cell line (Table 3, Fig. 1).

Discussion

Curcumin and quercetin are anticancer natural plant products targeting tumor cells in many cancer types such as lung, ovarian, colorectal, pancreatic, and BC [5, 22]. Recent studies showed that curcumin and quercetin can exert anti-tumorigenic activity through by effecting regulatory proteins such as transcription factors, receptors, enzymes, growth factors, cell cycle, and apoptosis-related molecules, as well as microRNAs [2, 5, 22]. However, the role of curcumin and quercetin on BC affecting the expression of miR-632 and miR-137 is not known completely.
Several miRNAs have been shown to affect BC cells. Also, they can be used as diagnostic or prognostic markers, and therapeutic targets in BC [22]. The curcumin treatment upregulates miR-181b, miR-34a, miR-16, miR-15a, and miR-146b-5p, and down-regulate miR-19a and –miR-19b in BC cell lines [22]. In addition, studies have shown that quercetin regulates many miRNAs related to proliferation (miR-302c, 26a, 503, 125a, 155, let-7 family, 195 and 215), apoptosis (miR-16, 26b, 34a, let-7g, 125a, 491 and –miR-605), tumor suppression (miR-125a 19b, 98,146a, 106a, 183, let-7 family and miR-381), metastasis and invasion (miR-146a/b, 503, and 194). Tao et al. investigated the quercetin anticancer effect in MDA-MB-231 and MCF-7 cells through the regulation of miR-146a [47, 48].
The knowledge of the miR-632 and miR-137 in tumor formation is controversial. The expression of miR-632 is high in hepatocellular carcinoma cells, and the downregulation of miR-632 suppresses proliferation and invasion of hepatocellular carcinoma cells targeting MYCT1 [39]. Contrary to this information, upregulation of miR-632 induced cell apoptosis and inhibited renal carcinoma cell growth and invasion [49, 50]. There are also different opinions on miR-137 function, It has been suggested the overexpression of miR-137 is inhibited cell apoptosis by reducing hypoxia-induced abnormal mitochondrial homeostasis and increased survival in breast cancer stem-like cells [46], but other reports claimed that miR-137 has been identified as a tumor suppressor in many cancer types [51, 52] such as laryngeal squamous cell carcinoma [44], pancreatic tumors [52]. In this study, we thought that miR-632 and miR-137 expressions were high in MCF-7 and MDA-MB-231 BC cell lines and that the overexpression of miR-632 and miR-137 in these cell lines was associated with the pathogenesis of breast cancer.
It’s known that curcumin has anti-cancer effects via regulating many miRNA expressions (e.g. miR-1, miR-7, –miR-9, miR-34a, miR-181, miR-21 and miR-19), but it has not been shown that curcumin could affect the cancer pathoge–nesis via miR-632. In this study, miR-632 expression is down-regulated in both MCF-7 and MDA-MB-231 breast cancer cell lines treated with curcumin compared to the untreated control groups, and we suggest that the reduction of –miR-632 treated with curcumin in these cell lines may relate with suppression of breast cancer progression. Mitra et al. showed that invasive and metastatic breast cancer cells express high levels of miR-632 compared to mammary epithelial cells, expression of miR-632 caused about a 2-fold increase in the invasive ability of the MCF10AT cells and revealed a 35% decrease in the invasive ability of these cells upon silencing miR-632 compared to the control-treated cells [30].
Quercetin is capable of inducing cytotoxic effects including inhibition of cell proliferation and apoptosis in human BC cells and regulates the expression of miRNAs. The inhibitor effect of quercetin was reported for miR-27a in renal cancer cells [53] and in colon cancer cells [54]. Tao et al. also reported that the quercetin inhibits cell proliferation in human BC cells modulating up-regulating miR-146a expression, then inducing apoptosis through caspase-3 activation and mitochondrial-dependent pathways, and inhibiting invasion through down-regulating the expression of EGFR [47]. We observed that miR-632 expression is down-regulated in both MCF-7 and MDA-MB-231 breast cancer cell lines treated with quercetin compared to the untreated control groups and we suggested that the reduction of miR-632 in these cells may be related with the inhibition of breast cancer progression.
In this study with the curcumin and quercetin treatment miR-137 expression was down-regulated in both MCF-7 and MDA-MB-231 BC cell lines compared to control groups. The decrease of the miR-137 expression is more prominent in the MCF-7 cell line of curcumin and quercetin treatment groups than the MDA-MB-231 groups. Ying et al. reported that elevated miR-137 levels in BC tissues correlated with decreased patient survival, overexpression of miR-137 markedly increased EMT and invasion, whereas its depletion, was shown to decrease EMT and invasion [45]. It has been shown that miR-137 decreases with neoadjuvant treatments in hormone receptor-positive breast cancer and the reduction of miR-137 can reduce BC aggression [55]. It’s known that the MCF-7 cell line has functional estrogen and EGF receptors is dependent on estrogen and EGF for growth, and is noninvasive, while MDA-MB-231 cells are a model for more aggressive, hormone-independent breast cancer, so decreases of –miR-137 is more effective in the MCF-7 group. However, Lee et al. also reported that miR-137 was significantly downregulated in triple-negative breast cancer tissues (TNBC), plasma, and the overexpression of miR-137 inhibited TNBC cell proliferation, invasion, and migration by decreasing Del-1 expression [56].

Conclusions

Studies have shown that there are conflicting data regarding miR-632 and miR-137 as oncogenes or tumor suppressors. In conclusion, our results demonstrated that curcumin and quercetin treatment decreased on the growth of MCF-7 and MDA-MB-231 human cancer breast cell line by down-regulating miR-137 and miR-632. This finding indicated that curcumin and quercetin may be used as a therapeutic agents and also miR-137 and miR632 are used in diagnosis, treatment efficacy, and prognosis in BC.
 
Received 16.01.2023
Revised 27.01.2023
Accepted 30.01.2023

Список литературы

  1. 1. Sung H., Ferlay J., Siegel R.L., Laversanne M., Soerjomataram I., Jemal A., Bray F. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA: Cancer J. Clin. 2021. 71. 209-249.
  2. 2. Farghadani R., Naidu R. Curcumin as an Enhancer of Thera–peutic Efficiency of Chemotherapy Drugs in Breast Cancer. Int. J. Mol. Sci. 2022 Feb 15. 23(4). 2144. doi: 10.3390/ijms23042144.
  3. 3. Askar M.A., El Shawi O.E., Abou Zaid O.A.R., Mansour N.A., Hanafy A.M. Breast cancer suppression by curcumin-naringenin-magnetic-nano-particles: in vitro and in vivo studies. Tumour Biol. 2021. 43(1). 225-247. doi: 10.3233/TUB-211506.
  4. 4. Tutar L., Özgür A., Tutar Y. Involvement of miRNAs and Pseudogenes in Cancer. Methods Mol. Biol. 2018. 1699. 45-66. doi: 10.1007/978-1-4939-7435-1_3.
  5. 5. Asgharian P., Tazekand A.P., Hosseini K., Forouhandeh H., Ghasemnejad T. et al. Potential mechanisms of quercetin in cancer prevention: focus on cellular and molecular targets. Cancer Cell. Int. 2022 Aug 15. 22(1). 257. doi: 10.1186/s12935-022-02677-w.
  6. 6. Hossain R., Sarkar C., Hassan S.M.H., Khan R.A., Arman M. et al. In silico screening of natural products as potential inhibitors of SARS-CoV-2 using molecular docking simulation. Chin. J. Integr. Med. 2021. 28. 1-8.
  7. 7. Islam M.S., Quispe C., Hossain R., Islam M.T., Al-Harrasi A. et al. Neuropharmacological effects of quercetin: a literature-based review. Front. Pharmacol. 2021. 12. 665031.
  8. 8. Shutenko Z., Henry Y., Pinard E., Seylaz J., Potier P. et al. Influence of the antioxidant quercetin in vivo on the level of nitric oxide determined by electron paramagnetic resonance in rat brain during global ischemia and reperfusion. Biochem. Pharmacol. 1999. 57(2). 199-208.
  9. 9. Chang W.-S., Lee Y., Lu F., Chiang H.-C. Inhibitory effects of flavonoids on xanthine oxidase. Anticancer Res. 1993. 13(6A). 2165-70.
  10. 10. Iio M., Ono Y., Kai S., Fukumoto M. Effects of flavonoids on xanthine oxidation as well as on cytochrome c reduction by milk xanthine oxidase. J. Nutr. Sci. Vitaminol. 1986. 32(6). 635-42.
  11. 11. Mandel S., Weinreb O., Amit T., Youdim M.B. Cell signaling pathways in the neuroprotective actions of the green tea polyphenol (–)-epigallocatechin-3-gallate: implications for neurodegenerative diseases. J. Neurochem. 2004. 88(6). 1555-69.
  12. 12. Rahman A., Hadi S.M., Parish J.H. Complexes involving quercetin, DNA and Cu(II). Carcinogenesis. 1990. 11(11). 2001-3.
  13. 13. Arai Y., Watanabe S., Kimira M., Shimoi K., Mochizuki R., Kinae N. Dietary intakes of flavonols, flavones and isoflavones by Japanese women and the inverse correlation between quercetin intake and plasma LDL cholesterol concentration. J. Nutr. 2000. 130(9). 2243-50.
  14. 14. Costantino L., Rastelli G., Gamberini M.C., Vinson J.A., Bose P. et al. 1-benzopyran-4-one antioxidants as aldose reductase inhibitors. J. Med. Chem. 1999. 42(11). 1881-93.
  15. 15. Soobrattee M.A., Bahorun T., Aruoma O.I. Chemopreventive actions of polyphenolic compounds in cancer. BioFactors. 2006. 27(1–4). 19-35.
  16. 16. Fotsis T., Pepper M.S., Aktas E., Breit S., Rasku S. et al. Flavonoids, dietary-derived inhibitors of cell proliferation and in vitro angiogenesis. Can. Res. 1997. 57(14). 2916-21.
  17. 17. Khan F., Niaz K., Maqbool F., Ismail Hassan F., Abdollahi M. et al. Molecular targets underlying the anticancer effects of quercetin: an update. Nutrients. 2016. 8(9). 529.
  18. 18. Alvi N.K., Rizvi R.Y., Hadi S.M. Interaction of quercetin with DNA. Biosci. Rep. 1986. 6(10). 861-8.
  19. 19. Rahman A., Hadi S.M., Parish J.H., Ainley K. Strand scission in DNA induced by quercetin and Cu(II): role of Cu(I) and oxygen free radicals. Carcinogenesis. 1989. 10(10). 1833-9.
  20. 20. Fazal F., Rahman A., Greensill J., Ainley K., Hadi S.M., Parish J.H. Strand scission in DNA by quercetin and Cu(II): identification of free radical intermediates and biological consequences of scission. Carcinogenesis. 1990. 11(11). 2005-8.
  21. 21. Guneydas G., Topcul M.R. Antiproliferative Effects of Curcumin Different Types of Breast Cancer. Asian Pac. J. Cancer Prev. 2022 Mar 1. 23(3). 911-917. doi: 10.31557/APJCP.2022.23.3.911.
  22. 22. Norouzi S., Majeed M., Pirro M., Generali D., Sahebkar A. Curcumin as an Adjunct Therapy and microRNA Modulator in Breast Cancer. Curr. Pharm. Des. 2018. 24(2). 171-177. doi: 10.2174/1381612824666171129203506.
  23. 23. Liu D., Chen Z. The effect of curcumin on breast cancer cells. J. Breast Cancer. 2013 Jun. 16(2). 133-7. doi: 10.4048/jbc.2013.16.2.133.
  24. 24. Roberts E., Cossigny D.A., Quan G.M. The role of vascular endothelial growth factor in metastatic prostate cancer to the skeleton. Prostate Cancer. 2013. 2013. 418340.
  25. 25. Farghadani R., Naidu R. Curcumin: Modulator of Key Molecular Signaling Pathways in Hormone-Independent Breast Cancer. Cancers. 2021. 13. 3427.
  26. 26. Chen J., Wang F.-L., Chen W.-D. Modulation of apoptosis-related cell signalling pathways by curcumin as a strategy to inhibit tumor progression. Mol. Biol. Rep. 2014. 41. 4583-4594.
  27. 27. Banik U., Parasuraman S., Adhikary A.K., Othman N.H. Curcumin: the spicy modulator of breast carcinogenesis. J. Exp. Clin. Cancer Res. 2017. 36. 98.
  28. 28. Mirzaei H., Masoudifar A., Sahebkar A., Zare N., Sadri Na–hand J. et al. MicroRNA: a novel target of curcumin in cancer therapy. J. Cell. Physiol. 2018 Apr. 233(4). 3004-3015. doi: 10.1002/jcp.26055.
  29. 29. Seki N., Hattori A., Hayashi A., Kozuma S., Miyajima N., Saito T. Cloning, tissue expression, and chromosomal assignment of human MRJ gene for a member of the DNAJ protein family. J. Hum. Genet. 1999. 44. 185-189.
  30. 30. Mitra A., Rostas J.W., Dyess D.L., Shevde L.A., Samant R.S. Micro-RNA-632 downregulates DNAJB6 in breast cancer. Lab. Invest. 2012 Sep. 92(9). 1310-7. doi: 10.1038/labinvest.2012.87.
  31. 31. Bartel D.P. MicroRNAs: genomics, biogenesis, mechanism, and function. Cell. 2004. 116. 281-97.
  32. 32. Mar-Aguilar F., Mendoza-Ramirez J.A., Malagon-Santiago I. et al. Serum circulating microRNA profiling for identification of potential breast cancer biomarkers. Dis. Markers. 2013. 34. 163-9.
  33. 33. Dumont N., Tlsty T.D. Reflections on miR-ing effects in metastasis. Cancer Cell. 2009 Jul 7. 16(1). 3-4. doi: 10.1016/j.ccr.2009.06.013.
  34. 34. Rameshwar P. Potential novel targets in breast cancer. Curr. Pharm. Biotechnol. 2009 Feb. 10(2). 148-53. doi: 10.2174/138920109787315024.
  35. 35. Wright J.A., Richer J.K., Goodall G.J. MicroRNAs and EMT in mammary cells and breast cancer. J. Mammary Gland Biol. Neoplasia. 2010 Jun. 15(2). 213-23. doi: 10.1007/s10911-010-9183-z.
  36. 36. O’Day E., Lal A. MicroRNAs and their target gene networks in breast cancer. Breast Cancer Res. 2010. 12(2). 201. doi: 10.1186/bcr2484.
  37. 37. Yu Z., Baserga R., Chen L., Wang C., Lisanti M.P., Pestell R.G. MicroRNA, cell cycle, and human breast cancer. Am. J. Pathol. 2010 Mar. 176(3). 1058-64. doi: 10.2353/ajpath.2010.090664.
  38. 38. Calin G.A., Croce C.M. MicroRNA-cancer connection: the beginning of a new tale. Cancer Res. 2006 Aug 1. 66(15). 7390-4. doi: 10.1158/0008-5472.CAN-06-0800.
  39. 39. Pu J., Wang J., Xu Z. et al. MiR-632 functions as oncogene in hepatocellular carcinoma via targeting MYCT1. Hum. Gene Therapy Clin. Dev. 2019. 30(2). 67-73.
  40. 40. Shi Y., Huang X., Chen G. et al. MiR-632 promotes gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner. BMC Cancer. 2019. 19(1). 14.
  41. 41. Cao Y.C., Song L.Q., Xu W.W., Qi J.J., Wang X.Y., Su Y. Serum miR-632 is a potential marker for the diagnosis and prognosis in laryngeal squamous cell carcinoma. Acta Otolaryngol. 2020 May. 140(5). 418-421. doi: 10.1080/00016489.2020.1717610.
  42. 42. Mahmoudi E., Cairns M.J. MiR-137: an important player in neural development and neoplastic transformation. Mol. Psychiatry. 2017 Jan. 22(1). 44-55. doi: 10.1038/mp.2016.150.
  43. 43. Fan W.H., Wang F.C., Jin Z., Zhu L., Zhang J.X. Curcumin Synergizes with Cisplatin to Inhibit Colon Cancer through Targeting the MicroRNA-137-Glutaminase Axis. Curr. Med. Sci. 2022 Feb. 42(1). 108-117. doi: 10.1007/s11596-021-2469-0.
  44. 44. Wan L., Gu D., Jin X. LncRNA NCK1-AS1 Promotes Malignant Cellular Phenotypes of Laryngeal Squamous Cell Carcinoma via miR-137/NCK1 Axis. Mol. Biotechnol. 2022 Aug. 64(8). 888-901. doi: 10.1007/s12033-022-00469-1.
  45. 45. Ying X., Sun Y., He P. MicroRNA-137 inhibits BMP7 to enhance the epithelial-mesenchymal transition of breast cancer cells. Oncotarget. 2017 Mar 14. 8(11). 18348-18358. doi: 10.18632/oncotarget.15442.
  46. 46. Hu Q., Yuan Y., Wu Y., Huang Y., Zhao Z., Xiao C. MicroRNA‑137 exerts protective effects on hypoxia‑induced cell injury by inhibiting autophagy/mitophagy and maintaining mitochondrial function in breast cancer stem‑like cells. Oncol. Rep. 2020 Oct. 44(4). 1627-1637. doi: 10.3892/or.2020.7714.
  47. 47. Tao S.F., He H.F., Chen Q. Quercetin inhibits proliferation and invasion acts by upregulating miR-146a in human breast cancer cells. Mol. Cell. Biochem. 2015 Apr. 402(1–2). 93-100. doi: 10.1007/s11010-014-2317-7.
  48. 48. Ahmed F., Ijaz B., Ahmad Z., Farooq N., Sarwar M.B., Husnain T. Modification of miRNA expression through plant extracts and compounds against breast cancer: mechanism and translational significance. Phytomedicine. 2020 Mar. 68. 153168. doi: 10.1016/j.phymed.2020.153168.
  49. 49. Jin L., Li Y., Zhang Z., He T., Hu J. et al. MiR-514a-3p functions as a tumor suppressor in renal cell carcinoma. Oncol. Lett. 2017. 14. 5624.
  50. 50. Xie R., Liu C., Liu L., Lu X., Tang G. Long non-coding RNA FEZF1-AS1 promotes rectal cancer progression by competitively bin–ding miR-632 with FAM83A. Acta Biochim. Biophys. Sin. (Shanghai). 2022 Apr 25. 54(4). 452-462. doi: 10.3724/abbs.2022022.
  51. 51. Li D., Shan W., Fang Y., Wang P., Li J. MiR-137 acts as a tumor suppressor via inhibiting CXCL12 in human glioblastoma. Oncotarget. 2017. 8. 101262-101270.
  52. 52. Wang Z.C., Huang F.Z., Xu H.B., Sun J.C., Wang C.F. MicroRNA-137 inhibits autophagy and chemosensitizes pancreatic cancer cells by targeting ATG5. Int. J. Biochem. Cell. Biol. 2019 Jun. 111. 63-71. doi: 10.1016/j.biocel.2019.01.020.
  53. 53. Li W., Liu M., Xu Y.F., Feng Y., Che J.P., Wang G.C., Zheng J.H. Combination of quercetin and hyperoside has anticancer effects on renal cancer cells through inhibition of oncogenic –microRNA-27a. Oncol. Rep. 2014 Jan. 31(1). 117-24. doi: 10.3892/or.2013.2811.
  54. 54. Del Follo-Martinez A., Banerjee N., Li X., Safe S., Mertens-Talcott S. Resveratrol and quercetin in combination have anticancer activity in colon cancer cells and repress oncogenic microRNA-27a. Nutr. Cancer. 2013. 65(3). 494-504. doi: 10.1080/01635581.2012.725194.
  55. 55. Ryspayeva D., Halytskiy V., Kobyliak N., Dosenko I., Fedosov A. et al. Response to neoadjuvant chemotherapy in breast cancer: do microRNAs matter? Discov. Oncol. 2022 Jun 7. 13(1). 43. doi: 10.1007/s12672-022-00507-z.
  56. 56. Lee S.J., Jeong J.H., Kang S.H., Kang J., Kim E.A., Lee J. et al. MicroRNA-137 inhibits cancer progression by targeting Del-1 in triple-negative breast cancer cells. International Journal of Molecular Sciences. 2019. 20(24). 6162.

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