Double‐negative feedback interaction between DNA methyltransferase 3A and microRNA‐145 in the Warburg effect of ovarian cancer cells

Zhang, Songlin; Pei, Meili; Li, Zhen; Li, Han; Li, Yanli; Li, Jie

doi:10.1111/cas.13734

Cited by 39 publications

(55 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We revealed miR-145 inhibited aerobic glycolysis through targeting HK2, and miR-145 downregulated PKM2 expression in our previous study; however, the specific mechanism remained unclear (Zhang et al, 2018). We found that miR-145 could upregulate the miR-133b mRNA level (Figure 2a).…”

Section: Upregulated Mir-133b Mediated Inhibitory Activity Of Mir-1mentioning

confidence: 63%

“…We have demonstrated that miR‐145 increased miR‐133b expression on a methylation level, and confirmed miR‐145 regulated PKM2 through miR‐133b. In our previous research, we showed that miR‐145 and DNMT3A formed negative feedback pathways (Zhang et al, ). In addition, we demonstrated that miR‐145 upregulated miR‐133b expression by targeting DNMT3A and c‐myc, thus downregulating the methylation level of the miR‐133b promoter region.…”

Section: Discussionmentioning

confidence: 98%

“…Normal ovarian tissue 2.8 | Glucose consumption and lactate production assay Methods described in previous studies (Zhang et al, 2018).…”

Section: Characteristics Casesmentioning

confidence: 99%

See 2 more Smart Citations

miR‐145 promotes miR‐133b expression through c‐myc and DNMT3A‐mediated methylation in ovarian cancer cells

Zhang

Zou

et al. 2019

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

Ovarian cancer presents as malignant tumors in the female reproductive system with high mortality. MicroRNAs are involved in the progression of ovarian cancer; however, the regulatory relationship among miRs remains unclear. In our study, we verified that both miR-145 and miR-133b messenger RNA (mRNA) levels in ovarian cancer tissues were lower than in normal ovarian tissues, and their mRNA level in serum of patients with ovarian cancer was reduced. We demonstrated miR-145 targeted c-myc, and c-myc interacted physically with DNMT3A in ovarian cancer cells. We confirmed that c-myc recruited DNMT3A to the miR-133b promoter. miR-133b overexpression also inhibited target gene PKM2 expression along with the Warburg effect. Our results indicate that miR-145 inhibited the Warburg effect through miR-133b/PKM2 pathways, which may improve approaches to ovarian cancer diagnosis and treatment. K E Y W O R D Sc-myc, DNMT3A, miR-133b, miR-145, ovarian cancer, Warburg effect

show abstract

Section: Upregulated Mir-133b Mediated Inhibitory Activity Of Mir-1mentioning

confidence: 63%

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

miR‐145 promotes miR‐133b expression through c‐myc and DNMT3A‐mediated methylation in ovarian cancer cells

Zhang

Zou

et al. 2019

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In recent years, the regulatory role of miR-145 in tumor metabolism has been paid more and more attention. In our previous studies, we found that miR-145 regulates Warburg effect by targeting HK2 (Zhang et al, 2018b). However, whether miR-145 is involved in glutamine metabolism and the clear molecular mechanism is not fully known.…”

Section: Discussionmentioning

confidence: 96%

miR‐145 inhibits glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells

et al. 2019

Cell Biology International

Self Cite

View full text Add to dashboard Cite

miR‐145 has been found to be a participant in cancer metastasis and glucose metabolism in ovarian cancer. However, the role of glutamine metabolism in ovarian cancer remains unclear. In this study, we aim to elucidate the molecular mechanism underlying the regulation of glutamine metabolism by miR‐145 in ovarian cancer cells. The messenger RNA (mRNA) levels of miR‐145 and glutaminase 1 (GLS1) were examined by quantitative real‐time polymerase chain reaction (qRT‐PCR). The protein levels of c‐myc and GLS1 were detected by western blot analysis. Luciferase reporter assays were used to validate c‐myc was a target of miR‐145. Glutamine metabolism was analyzed using assay kits. In addition, we performed luciferase reporter assays and chromatin immunoprecipitation assay to validate c‐myc transcription activated GLS1 and promoted GLS1 expression. The qRT‐PCR demonstrated that the mRNA level of miR‐145 and GLS1 was negatively correlated in ovarian cancer tissues and cell lines. Kaplan–Meier survival analysis and the log‐rank test showed that patients with high miR‐145 expression had significantly increased the overall survival. The overexpression of miR‐145 inhibited glutamine consumption, α‐ketoglutarate production, and cellular ATP levels. Furthermore, we found miR‐145 inhibited glutamine metabolism by targeting c‐myc. Moreover, c‐myc could promote GLS1 expression by transcription activated. Together, our results revealed that miR‐145 inhibited glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells, which may improve the current strategy of ovarian cancer diagnosis and therapy.

show abstract

“…In osteosarcoma, micelleplexes containing miR‐145 are used to suppress cell proliferation and migration . In ovarian cancer, the negative feedback loop of DNMT3A and miR‐145 can affect the Warburg effect of cells . MiR‐145 has also been used to treat prostate cancer metastasis .…”

Section: Introductionmentioning

confidence: 99%

MiR‐145‐targeted HBXIP modulates human breast cancer cell proliferation

et al. 2018

View full text Add to dashboard Cite

BackgroundMiR‐145 has been identified as a tumor suppressive microRNA in multiple cancers. In this current investigation, we searched for new direct targets of miR‐145 and evaluated their effect on breast cancer development.MethodsTargetscan was used to predict the target genes of miR‐145. The targeting of miR‐145 on oncogenic HBXIP was verified by luciferase reporter gene analysis. The effect of miR‐145 on the level of messenger RNA and protein of HBXIP was evaluated by quantitative real‐time PCR and immunoblotting. Correlations between miR‐145 and HBXIP, as well as miR‐145 expression, were analyzed in 30 paired breast cancer and noncancerous tissues by quantitative real‐time PCR. Methyl thiazol tetrazolium and colony formation assays were applied to determine the cell proliferation ability.Results HBXIP was identified as a novel target gene of miR‐145 in breast cancer. MiR‐145 was found to dose‐dependently decrease messenger RNA and protein expression of HBXIP in breast cancer MCF‐7 cells. Notably, miR‐145 expression was negatively related to HBXIP expression and was obviously reduced in breast cancer samples. Finally, miR‐145 suppressed cell proliferation while its inhibitor, anti‐miR‐145, accelerated cell proliferation. Interestingly, silencing of HBXIP reversed the acceleration of cell proliferation induced by anti‐miR‐145 in breast cancer.ConclusionOncogenic HBXIP is a new direct target of tumor suppressive miR‐145. Our findings reveal that miR‐145‐targeting HBXIP could be a potential therapeutic target in breast cancer.

show abstract

Double‐negative feedback interaction between DNA methyltransferase 3A and microRNA‐145 in the Warburg effect of ovarian cancer cells

Cited by 39 publications

References 37 publications

miR‐145 promotes miR‐133b expression through c‐myc and DNMT3A‐mediated methylation in ovarian cancer cells

miR‐145 promotes miR‐133b expression through c‐myc and DNMT3A‐mediated methylation in ovarian cancer cells

miR‐145 inhibits glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells

MiR‐145‐targeted HBXIP modulates human breast cancer cell proliferation

Contact Info

Product

Resources

About