scholarly journals miR-454 suppresses the proliferation and invasion of ovarian cancer by targeting E2F6

2020 ◽  
Author(s):  
Yunhe An ◽  
Jun Zhang ◽  
Yanjie Tian ◽  
Baoming Li ◽  
Xiaoyan Cheng ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Reporter Assay ◽  
Cancer Tissues ◽  
Dual Luciferase Reporter Assay

Abstract Background The aberrant expression of microRNA-454 (miR-454) has been confirmed to be involved in the development of cancers. However, the functional role of miR-454 in the progression of ovarian cancer remains unclear. Methods The expression of miR-454 in ovarian cancer cells and serum of ovarian cancer patients was detected by RT-PCR. CCK8, colony formation, transwell, and flow cytometry assays were conducted to assess the effects of miR-454 on ovarian cancer cell proliferation, migration, invasion, and apoptosis, respectively. Dual-luciferase reporter assay was used to confirm the targeting relationship between miR-454 and E2F6. The expression pattern of E2F6 in ovarian cancer tissues was detected using immunohistochemistry (IHC) assay. The relative expression of related proteins was examined using western blot analysis. Results miR-454 was markedly down-regulated by hypoxia in ovarian cancer cells. Compared with normal samples, the expression of miR-454 was up-regulated in the serum of ovarian cancer patients, and correlated with the clinicopathological stages of ovarian cancer. Next, we found that miR-454 overexpression inhibited the proliferation, migration and invasion of OVCAR3 and SKOV3 cells, as well as promoted apoptosis. In addition, the Akt/mTOR and Wnt/β-catenin signaling pathway were inhibited by miR-454 in ovarian cancer cells. Mechanically, bioinformatic analysis and dual-luciferase reporter assay confirmed that E2F6 was a direct target of miR-454 and negatively regulated by miR-454 in ovarian cancer cells. Moreover, IHC analysis showed that E2F6 was highly expressed in ovarian cancer tissues. Finally, we found that the increasing cell proliferation and migration triggered by E2F6 overexpression were abolished by miR-454 overexpression. Conclusion Taken together, these results highlight the role of miR-454 as a tumor suppressor in ovarian cancer cells by targeting E2F6, indicating that miR-454 may be a potential diagnostic biomarker and therapeutic target for ovarian cancer.

scholarly journals miR-454 suppresses the proliferation and invasion of ovarian cancer by targeting E2F6

2020 ◽  
Author(s):  
Yunhe An ◽  
Jun Zhang ◽  
Yanjie Tian ◽  
Baoming Li ◽  
Xiaoyan Cheng ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Reporter Assay ◽  
Cancer Tissues ◽  
Dual Luciferase Reporter Assay

Abstract Background: It has been reported that hypoxia is closely related to the tumor malignancy and recurrence and regulates multiple hub genes in ovarian cancer. MicroRNA-454 (miR-454) has been confirmed to be involved in tumorigenesis and tumor development. However, the functional role of miR-454 in ovarian cancer remains unclear.Methods: The expression of miR-454 in ovarian cancer cells and serum of ovarian cancer patients was detected by RT-PCR. CCK8, colony formation, transwell, and flow cytometry assays were conducted to assess the effects of miR-454 on ovarian cancer cell proliferation, migration, invasion, and apoptosis. Dual-luciferase reporter assay was used to confirm the targeting relationship between miR-454 and E2F6. The expression pattern of E2F6 in ovarian cancer tissues was detected using immunohistochemistry assay. The relative expression of related proteins was examined using western blot analysis.Results: miR-454 was markedly down-regulated by hypoxia in ovarian cancer cells. Compared with normal serum, the expression of miR-454 was up-regulated in the serum of ovarian cancer patients, and was correlated with the clinicopathological stage of ovarian cancer patients. Next, we found that miR-454 overexpression inhibited the proliferation, migration and invasion of OVCAR3 and SKOV3 cells, as well as promoted apoptosis. In addition, the Akt/mTOR and Wnt/β-catenin signaling pathway were inhibited by miR-454. Bioinformatic analysis and dual-luciferase reporter assay confirmed that E2F6 was a target of miR-454 and negatively regulated by miR-454 in ovarian cancer cells. Moreover, immunohistochemical analysis showed that E2F6 was highly expressed in ovarian cancer tissues. Finally, we found that the increasing cell proliferation and migration triggered by E2F6 overexpression were abolished by miR-454 overexpression.Conclusion: Taken together, these results highlight the role of miR-454 as a tumor suppressor in ovarian cancer by targeting E2F6, indicating that the hypoxia/miR-454/E2F6 pathway may be a novel therapeutic approach for ovarian cancer.

scholarly journals circRNA-UBAP2 promotes the proliferation and inhibits apoptosis of ovarian cancer though miR-382-5p/PRPF8 axis

2020 ◽  
Author(s):  
Qin Xu ◽  
Bo Deng ◽  
Manlin Li ◽  
Yang Chen ◽  
Li Zhuan
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Target Gene ◽  
Circular Rnas ◽  
Ovarian Cancer Cells ◽  
Competing Endogenous Rnas ◽  
Cancer Tissues

Abstract Objective: circular RNAs (circRNAs) have been reported to be essential regulators of multiple malignant cancers. However, the functions of circRNAs in ovarian cancer need to be further explored. The aim of our study is to explore the role of circRNA-UBAP2 in ovarian cancer and its mechanism. Results: circRNA-UBAP2 was upregulated in ovarian cancer tissues and cell lines. Knockdown of circRNA-UBAP2 inhibited cell proliferation and promoted cell apoptosis, but circRNA-UBAP2 overexpressed got opposite results. In addition, circRNA-UBAP2 targeted miR-382-5p and downregulated its expression, PRPF8 was a target gene of miR-382-5p. Furthemore, circRNA-UBAP2/miR-382-5p/PRPF8 axis affected the proliferation, apoptosis and cell cycle of ovarian cancer through the mechanism of competing endogenous RNAs (ceRNA). Conclusion: circRNA-UBAP2 acted as a ceRNA to sponged miR-382-5p, increased the expression level of PRPF8, and prompted proliferation and inhibited apoptosis in ovarian cancer cells.

scholarly journals circRNA-UBAP2 promotes the proliferation and inhibits apoptosis of ovarian cancer though miR-382-5p/PRPF8 axis

2020 ◽  
Author(s):  
Qin Xu ◽  
Bo Deng ◽  
Manlin Li ◽  
Yang Chen ◽  
Li Zhuan
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Target Gene ◽  
Circular Rnas ◽  
Ovarian Cancer Cells ◽  
Competing Endogenous Rnas ◽  
Cancer Tissues

Abstract Objective: circular RNAs (circRNAs) have been reported to be essential regulators of multiple malignant cancers. However, the functions of circRNAs in ovarian cancer need to be further explored. The aim of our study is to explore the role of circRNA-UBAP2 in ovarian cancer and its mechanism. Results: circRNA-UBAP2 was upregulated in ovarian cancer tissues and cell lines. Knockdown of circRNA-UBAP2 inhibited cell proliferation and promoted cell apoptosis, but circRNA-UBAP2 overexpressed got opposite results. In addition, circRNA-UBAP2 targeted miR-382-5p and downregulated its expression, PRPF8 was a target gene of miR-382-5p. Furthemore, circRNA-UBAP2/miR-382-5p/PRPF8 axis affected the proliferation, apoptosis and cell cycle of ovarian cancer through the mechanism of competing endogenous RNAs (ceRNA). Conclusion: circRNA-UBAP2 acted as a ceRNA to sponged miR-382-5p, increased the expression level of PRPF8, and prompted proliferation and inhibited apoptosis in ovarian cancer cells.

scholarly journals LncRNA GAS5 suppresses ovarian cancer by inducing inflammasome formation

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Jie Li ◽  
Chen Yang ◽  
Yinguang Li ◽  
Aiyue Chen ◽  
Li Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Colony Formation ◽  
Sandwich Elisa ◽  
Ovarian Cancer Cells ◽  
Cancer Tissues ◽  
Lncrna Gas5

Objective: Long noncoding RNA growth arrest-specific transcript 5 (lncRNA GAS5) is involved in various kinds of cancer. However, the role of lncGAS5 in the development of ovarian cancer remains unclear. In the present study, we explored the cellular mechanism and clinical value of lncRNA GAS5 in ovarian cancer. Methods: Quantitative real-time PCR was used to detect mRNA level of lncRNA GAS5 in 20 ovarian cancer tissues. The effect of lncRNA GAS5 on cell proliferation was performed using CCK-8 assay. Cell apoptosis was evaluated by flow cytometry. Western blotting was used to detect the protein level of lncRNA GAS5 potential target. Standard sandwich ELISA was used to quantify the level of inflammatory cytokines. The cells with stable expression of lncRNA GAS5 were injected into nude mice to study the effect of lncRNA GAS5 on tumorigenesis in vivo. Results: The expression of lncRNA GAS5 was significantly decreased in ovarian cancer tissues. Decrease in lncRNA GAS5 expression resulted in increased cell proliferation and colony formation and reduced ovarian cancer cell apoptosis. In contrast, exogenous overexpression of lncRNA GAS5 in ovarian cancer cells inhibited proliferation, colony formation, and apoptosis in ovarian cancer cells. In addition, the role of lncRNA GAS5 in ovarian cancer was associated with inflammasome formation and pyroptosis. Conclusion: These results suggested that lncRNA GAS5 acts as tumor suppressor and could be used as a potential treatment target for diagnosis and therapy of ovarian cancer.

scholarly journals Ginsenoside 20(S)-Rg3 Prevents PKM2-Targeting miR-324-5p from H19 Sponging to Antagonize the Warburg Effect in Ovarian Cancer Cells

2018 ◽  
Vol 51 (3) ◽  
pp. 1340-1353 ◽  
Author(s):  
Xia Zheng ◽  
Yuanyuan Zhou ◽  
Wei Chen ◽  
Lihong Chen ◽  
Jiaojiao Lu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Warburg Effect ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Reporter Assay ◽  
Dual Luciferase Reporter Assay ◽  
The Warburg Effect

Background/Aims: The Warburg effect is one of the main metabolic features for cancers, with long non-coding RNA (lncRNA) being involved as a class of crucial regulators. Our previous studies have shown that ginsenoside 20(S)-Rg3, an active saponin monomer extracted from red ginseng, inhibits the Warburg effect in ovarian cancer cells. However, the detailed lncRNA regulatory network modulated by 20(S)-Rg3 to prevent the Warburg effect in ovarian cancer cells has not been explored. Methods: High-throughput sequencing was used to screen out the differentially expressed lncRNAs between 20(S)-Rg3-treated and non-treated SKOV3 cells. The levels of lncRNA H19 and miR-324-5p were manipulated in SKOV3 and A2780, and the glucose consumption, lactate production and PKM2 protein level were detected. Dual-luciferase reporter assay and RIP were utilized to verify the direct binding of H19 to miR-324-5p and miR-324-5p to PKM2. Cell proliferation was examined by CCK8 and colony formation assay. Nude mice subcutaneous xenograft tumor models were established to evaluate the impact of miR-324-5p on tumor growth in vivo. Results: 20(S)-Rg3 downregulated 67 lncRNAs, and H19 was one of the most decreased lncRNAs. Suppression of H19 by siRNA transfection reduced glucose consumption, lactate production and PKM2 expression in ovarian cancer cells, while H19 overexpression in 20(S)-Rg3-treated ovarian cancer cells enhanced glucose consumption, lactate production and PKM2 expression. Dual-luciferase reporter assay and RIP results showed that H19 directly bound to miR-324-5p. Dual-luciferase reporter assay showed that miR-324-5p directly targeted PKM2, and miR-324-5p negatively regulated glucose consumption and lactate production in ovarian cancer cells. miR-324-5p overexpression inhibited cell proliferation in vitro and in vivo. Conclusion: Our study revealed that 20(S)-Rg3 blocked the competitive inhibition of H19 on miR-324-5p, which enhanced the suppression of miR-324-5p on PKM2 and therefore inhibited the Warburg effect and repressed tumorigenesis. In a word, 20(S)-Rg3 inhibited the Warburg effect in ovarian cancer cells via H19/miR-324-5p/PKM2 pathway.

lncRNA NEAT1 Inhibits Proliferation, Invasion and Epithelial-mesenchymal Transition of Gastric Cancer Cells by Regulating MiR-129-5p/PBX3 Axis

2020 ◽  
Author(s):  
Hanshu Ji ◽  
Xiaoyu Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Gastric Cancer Cells ◽  
Mesenchymal Transition ◽  
Lncrna Neat1 ◽  
Dual Luciferase Reporter Assay

Abstract Purpose: lncRNA NEAT1 has been reported as a tumor-promoting gene in a variety of tumors, but few studies have explored its role and mechanism in gastric cancer. In the face of increasing incidence of gastric cancer, how to improve the diagnostic accuracy and therapeutic effect of gastric cancer is a major clinical problem. Therefore, we studied the effect and mechanism of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition of gastric cancer cells. To inquiry into the effect of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer (GC) cells by regulating miR-129-5p/PBX3 axis. Methods: Totally 63 GC diagnosed and treated in our hospital were selected as the study subjects, whose paired GC tissues and pericarcinomatous tissues were collected as the study specimens after obtaining their consent. QRT-PCR was employed to detect the NEAT1 expression in tissues and cells to analyze the relationship between NEAT1 and clinicopathological data of GC patients. In addition, stable and transient overexpression and inhibition vectors were established and transfected into GC cells HCG-27 and MKN-45. CCK-8, traswell, and flow cytometry were employed to evaluate the proliferation, invasion, and apoptosis of transfected cells. The correlation of miR-129-5p between PBX3 and NEAT1 was assessed using dual luciferase reporter assay, while that between NEAT1 and miR-129-5p was assessed by RNA-binding protein immunoprecipitation (RIP) . Western blot was applied for the detection of apoptosis and EMT related proteins.Results: NEAT1 was overexpressed in GC patients and had a high diagnostic value. The expression of NEAT1 was related to the pathological stage, differentiation degree, tumor size and lymph node metastasis of patients with GC. Down-regulated NEAT1 brought decreased cell proliferation, invasion and EMT, and increased apoptosis. According to dual luciferase reporter assay, NEAT1 could target miR-129-5p, while in turn miR-129-5p could target PBX3. Functional analysis exhibited that miR-129-5p overexpression inhibited PBX3 in GC cells, affecting cell proliferation, invasion, EMT and apoptosis, and rescue experiments demonstrated that these effects were eliminated by up-regulating NEAT1 expression.Conclusion: Inhibition of NEAT1 could mediate miR-129-5p/PBX3 axis to promote apoptosis of GC cells, and reduce cell proliferation, invasion and EMT.

scholarly journals Demethoxycurcumin inhibited human epithelia ovarian cancer cells’ growth via up-regulating miR-551a

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769430 ◽  
Author(s):  
Zhenhua Du ◽  
Xianqun Sha
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Natural Form ◽  
Ovarian Cancer Cell Lines ◽  
Induced Apoptosis ◽  
Tumor Suppressive Function ◽  
Cancer Tissues

Curcumin is a natural agent that has ability to dampen tumor cells’ growth. However, the natural form of curcumin is prone to degrade and unstable in vitro. Here, we demonstrated that demethoxycurcumin (a curcumin-related demethoxy compound) could inhibit cell proliferation and induce apoptosis of ovarian cancer cells. Moreover, IRS2/PI3K/Akt axis was inactivated in cells treated with demethoxycurcumin. Quantitative real-time reverse transcription polymerase chain reaction demonstrated that miR-551a was down-regulated in ovarian cancer tissues and ovarian cancer cell lines. Over-expression of miR-551a inhibited cell proliferation and induced apoptosis of ovarian cancer cells, whereas down-regulation of miR-551a exerted the opposite function. Luciferase assays confirmed that there was a binding site of miR-551a in IRS2, and we found that miR-551a exerted tumor-suppressive function by targeting IRS2 in ovarian cancer cells. Remarkably, miR-551a was up-regulated in the cells treated with demethoxycurcumin, and demethoxycurcumin suppressed IRS2 by restoration of miR-551a. In conclusion, demethoxycurcumin hindered ovarian cancer cells’ malignant progress via up-regulating miR-551a.

miR-9-5p Increases Sensitivity to Cisplatin in Thyroid Cancer Cells by Down-Regulating BRAF Expression

2019 ◽  
Vol 9 (6) ◽  
pp. 751-759
Author(s):  
Wanzhi Chen ◽  
Jichun Yu ◽  
Rong Xie ◽  
Meijun Zhong
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Cell Number ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Thyroid Cancer Cells ◽  
Dual Luciferase Reporter Assay

Objective: To explore the expression of miR-9-5p and BRAF in cisplatin resistant strain thyroid cancer cells and reversal effect of drug resistance as well as the possible mechanism. Methods: The cisplatin-resistant thyroid cancer cells (FTC-133/DDP and TPC-1/DDP) were respectively divided into 3 groups as NC, DDP and DDP + miRNA groups. Measuring cell proliferation by MTT assay and cell apoptosis by flow cytometry; Evaluating invasion cell number and wound healing rates by transwell and wound healing assay. The relative proteins (BRAF, Mek and Erk1/2) were measured by WB assay. The correlation between miR-9-5p and BRAF by dual-luciferase reporter assay in FTC-133/DDP and TPC-1/DDP cells. Results: In FTC-133/DDP and TPC-1/DDP cells experiment, compared with DDP group, with miR-9-5p supplement, the cell proliferation rats were significantly depressed with cell apoptosis increasing (P < 0.001, respectively); invasion cell number and wound healing rats were significantly down-regulation (P < 0.001, respectively) in DDP + miRNA groups. Meanwhile, the BRAF, Mek and Erk1/2 proteins expressions were significantly depressed in DDP + miRNA groups were significantly suppressed compared with those in DDP groups (P < 0.001, respectively). By dual-luciferase reporter assay, BRAF was the target gene of miR-9-5p in FTC133/DDP and TPC-1/DDP cells. Conclusion: miR-9-5p increases sensitivity to cisplatin in thyroid cancer cells by down-regulating BRAF expression.

scholarly journals miR-4461 Regulates the Proliferation and Metastasis of Ovarian Cancer Cells and Cisplatin Resistance

2021 ◽  
Vol 11 ◽  
Author(s):  
Lei Dou ◽  
Yi Zhang
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Obvious Effect ◽  
Proliferation And Metastasis ◽  
Direct Target ◽  
Cancer Tissues ◽  
And Control

microRNAs (miRNAs) are of great significance in cancer treatment, which may have a desirable result on the regulation of tumorigenesis, progression, recurrence, and chemo-resistance of ovarian cancer. However, the research on the further potential application of miR-4461 in ovarian cancer is little and limited. Therefore, the study in this paper focus on the investigation of the of miR-4461 in ovarian cancer progression and chemo-resistance. The phenomenon that the proliferation and metastasis of ovarian cancer cells can be promoted by miR4461 is revealed in functional assays. Through the bioinformatics and luciferase reporter analysis, the PTEN is validated to be the direct target of miR-4461 in ovarian. The association between the expression of miR-4461 and PTEN is negative in in human ovarian cancer tissues. The distinction of growth and metastasis capacity between miR-4461 knockdown ovarian cancer cells and control cells is partially abolished by si-PTEN. Moreover, it was found that cisplatin treatment has obvious effect on the miR-4461 knockdown ovarian cancer cells. In summary, the data given in this paper indicate that the miR-4461 can be regarded as a potential onco-miRNA in ovarian cancer by targeting PTEN.

scholarly journals Ginsenoside 20(S)-Rg3 Inhibits the Warburg Effect Via Modulating DNMT3A/ MiR-532-3p/HK2 Pathway in Ovarian Cancer Cells

2018 ◽  
Vol 45 (6) ◽  
pp. 2548-2559 ◽  
Author(s):  
Yuanyuan Zhou ◽  
Xia Zheng ◽  
Jiaojiao Lu ◽  
Wei Chen ◽  
Xu Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Warburg Effect ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Skov3 Cells ◽  
Dual Luciferase Reporter Assay ◽  
The Warburg Effect

Background/Aims: The Warburg effect is one of the main energy metabolism features supporting cancer cell growth. 20(S)-Rg3 exerts anti-tumor effect on ovarian cancer partly by inhibiting the Warburg effect. microRNAs are important regulators of the Warburg effect. However, the microRNA regulatory network mediating the anti-Warburg effect of 20(S)-Rg3 was largely unknown. Methods: microRNA deep sequencing was performed to identify the 20(S)-Rg3-influenced microRNAs in SKOV3 ovarian cancer cells. miR-532-3p was overexpressed by mimic532-3p transfection in SKOV3 and A2780 cells or inhibited by inhibitor532-3p transfection in 20(S)-Rg3-treated cells to examine the changes in HK2 and PKM2 expression, glucose consumption, lactate production and cell growth. Dual-luciferase reporter assay was conducted to verify the direct binding of miR-532-3p to HK2. The methylation status in the promoter region of pre-miR-532-3p gene was examined by methylation-specific PCR. Expression changes of key molecules controlling DNA methylation including DNMT1, DNMT3A, DNMT3B, and TET1-3 were examined in 20(S)-Rg3-treated cells. DNMT3A was overexpressed in 20(S)-Rg3-treated cells to examine its influence on miR-532-3p level, HK2 and PKM2 expression, glucose consumption and lactate production. Results: Deep sequencing results showed that 11 microRNAs were increased and 9 microRNAs were decreased by 20(S)-Rg3 in SKOV3 cells, which were verified by qPCR. More than 2-fold increase of miR-532-3p was found in 20(S)-Rg3-treated SKOV3 cells. Forced expression of miR-532-3p reduced HK2 and PKM2 expression, glucose consumption and lactate production in SKOV3 and A2780 ovarian cancer cells. Inhibition of miR-532-3p antagonized the suppressive effect of 20(S)-Rg3 on HK2 and PKM2 expression, glucose consumption and lactate production in ovarian cancer cells. Dual-luciferase reporter assay showed that miR-532-3p directly suppressed HK2 rather than PKM2. miR-532-3p level was controlled by the methylation in the promoter region of its host gene. 20(S)-Rg3 inhibited DNMT3A expression while exerted insignificant effect on DNMT1, DNMT3B and TET1-3. 20(S)-Rg3 reversed DNMT3A-mediated methylation in the promoter of the host gene of miR-532-3p, and thus elevated miR-532-3p level followed by suppression of HK2 and PKM2 expression, glucose consumption and lactate production. Conclusions: 20(S)-Rg3 modulated microRNAs to exert the anti-tumor effect in ovarian cancer. 20(S)-Rg3 lessened the DNMT3A-mediated methylation and promoted the suppression of miR-532-3p on HK2 to antagonize the Warburg effect of ovarian cancer cells.

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