Effect of quercetin's anti-breast cancer depending on presence of estrogen receptor via down-regulating long non-coding RNA MALAT-1 and its mechanism

Zi-yi Zhao; Ming Xiongxiao; Cui-wei Zhang; Ming Xiongxiao; Cui-wei Zhang; Yu-peng Xie; Yi-wen Zhang

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Effect of quercetin's anti-breast cancer depending on presence of estrogen receptor via down-regulating long non-coding RNA MALAT-1 and its mechanism

Author: Zi-Yi ZHAO ¹ ; Ming XIONGXIAO ² ; Cui-Wei ZHANG ² ; Ming XIONGXIAO ³ ; Cui-Wei ZHANG ³ ; Yu-Peng XIE ⁴ ; Yi-Wen ZHANG ⁵
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1. TCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine
2. Dept of Pathology, the Affiliated Hospital of Southwest Medical University
3. Precision Pathology Diagnosis for Serious Diseases Key Laboratory of Luzhou
4. Clinical Medicine School of Southwest Medical University
5. State Key Laboratory of Biotherapy, West China Hospital
Publication Type:Journal Article
Keywords: 17p-estradiol; breast cancer; cell proliferation; estrogen receptor; MALAT-1; quercetin
From: Chinese Pharmacological Bulletin 2024;40(3):499-505
CountryChina
Language:Chinese
Abstract: Aim To investigate the molecular mechanism by which quercetin inhibits the malignant behavior of breast cancer cells. Methods Breast cancer cell lines MCF-7 and MB231 were used as the research models. Lentiviral transfection was employed to establish tumor cells with high expression of ERa and MAL-AT-1. The expression of MALAT-1 was assessed using RT-qPCR,and ERa expression was determined through Western blot. Subsequently, CCK-8 assay and colony formation assay were conducted to evaluate cell proliferation. PI staining and adenovirus transfection were performed to observe the inhibitory effects of quercetin on breast cancer cell proliferation. Results 17|3-es-tradiol ( E2 ) promoted the proliferation of MCF-7 breast cancer cells, while 5 jjunol L quercetin reversed the promoting effect of E2 on proliferation ( P 0. 05 ) . Quercetin had no effect on MB231 breast cancer cells. Overexpression of ERa significantly inhibited the pro-proliferative effect of E2 on MB231-ERa cells, and quercetin further suppressed this effect. Additionally , quercetin inhibited the expression of MALAT-1. However,this inhibitory effect was reversed by overexpression of MALAT-1, leading to enhanced cell proliferation , cell cycle progression, and clonal formation a-bility. Conclusions Quercetin exerts its anti-tumor effects on breast cancer cells by regulating MALAT-1, dependent on the presence of estrogen receptor. Quercetin shows potential as a therapeutic drug for breast cancer targeting the estrogen receptor.