miR-145 and miR-497 suppress TGF-β-induced epithelial–mesenchymal transition of non-small cell lung cancer by targeting MTDH

Yin, Qi; Han, Yu; Zhu, Dongyi; Li, Zhanxia; Shan, Shan; Jin, Wenjing; Lu, Qingchun; Ren, Tao

doi:10.1186/s12935-018-0601-4

Cited by 46 publications

(35 citation statements)

References 36 publications

(36 reference statements)

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“…miR‐145 is a newly discovered miRNA, which is significantly less expressed in breast cancer (Ding et al, ), cervical cancer (Sathyanarayanan et al, ), glioma (Xu et al, ), colon cancer (Li et al, ), esophageal cancer (Zhang et al, ), and non‐small‐cell lung cancer (Yin et al, ). The genes regulated by miRNA‐145 are different in different tumors, and the molecular mechanisms of their anti‐cancer effects are also different.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2019

Cell Biology International

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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.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2019

Cell Biology International

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“…Up to now, miRNAs have been revealed that they are involved in a large amount of biological processes, including tumour formation and inflammatory responses in many human diseases [25][26][27]. It is well known that miR-199a-5p has been studied to take part in the progress of cancer [28].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

Chi

Yang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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2020) Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-ABSTRACT Background: Glioblastoma multiforme (GBM) is one of the most prevailing primary brain tumours among adults and most aggressive cancers. Despite multiple developments in medical and surgical treatments, GBM is still a deadly disease with a high mortality rate. Here, this study was performed to investigate the function of circPVT1 on GBM. Methods: CCK-8 and flow cytometry were utilised to estimate viability and apoptosis in both cells. qRT-PCR was performed to determine circPVT1 and miR-199a-5p expression. Western blot was conducted to determine apoptosis, migration and EMT-related proteins levels when silencing circPVT1. Subsequently, these parameters were re-tested after up-regulating miR-199a-5p. Results: CircPVT1 was highly expressed in GBM tissues. Silencing circPVT1 raised two cells apoptosis and reduced viability and migration capacity. Moreover, EGF-induced EMT was repressed by silencing circPVT1. In addition, miR-199a-5p expression was elevated when silencing circPVT1. And silencing circPVT1 exerted above changes via up-regulating miR-199a-5p. Finally, silencing circPVT1 repressed YAP1 and PI3K/AKT pathways via up-regulating miR-199a-5p. Conclusion: Our data suggested that silencing circPVT1 inhibited viability, migration, EGF-induced EMT and promoted apoptosis as well as repressed YAP1 and PI3K/AKT pathways by up-regulating miR-199a-5p. HIGHLIGHTS 1. CircPVT1 expression is highly expressed in GBM tissues; 2. Si-circPVT1 represses migration and promoted apoptosis in U539 and U251 cells; 3. Si-circPVT1 represses migration and promoted apoptosis when elevating miR-199a-5p; 4. Si-circPVT1 represses EGF-induced EMT when increasing miR-199a-5p; 5. Si-circPVT1 suppresses YAP1 and PI3K/AKT pathways by up-regulating miR-199-5p. ARTICLE HISTORY

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“…Furthermore, the upregulation of miR‐183‐5p induced apoptosis and inhibited EMT, proliferation, invasion, and migration by the downregulation of ezrin in human endometrial cancer cells . Collectively, EMT is inhibited by many miRNAs, including miR‐145, miR‐497, miR‐145‐5p, miR‐138, miR‐200a, miR‐200b, miR‐655, miR‐30‐5p, and miR‐32 . In addition, EMT is also promoted by many miRNAs, including miR‐221, miR‐222, miR‐214‐3p, and miR‐181a …”

Section: Small Molecules Against Emtmentioning

confidence: 99%

“…194 Collectively, EMT is inhibited by many miRNAs, including miR-145, miR-497, miR-145-5p, miR-138, miR-200a, miR-200b, miR-655, miR-30-5p, and miR-32. [195][196][197][198][199][200][201] In addition, EMT is also promoted by many miRNAs, including miR-221, miR-222, miR-214-3p, and miR-181a. [202][203][204] The flavonoids rhamnetin from cloves, berries and cirsiliol from Cirsium lineare (Thunb.)…”

Section: Ras Signaling Pathwaymentioning

confidence: 99%

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

Feng

Chen

Vaziri

et al. 2019

Medicinal Research Reviews

109

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Tissue fibrosis and cancer both lead to high morbidity and mortality worldwide; thus, effective therapeutic strategies are urgently needed. Because drug resistance has been widely reported in fibrotic tissue and cancer, developing a strategy to discover novel targets for targeted drug intervention is necessary for the effective treatment of fibrosis and cancer. Although many factors lead to fibrosis and cancer, pathophysiological analysis has demonstrated that tissue fibrosis and cancer share a common process of epithelial‐mesenchymal transition (EMT). EMT is associated with many mediators, including transcription factors (Snail, zinc‐finger E‐box‐binding protein and signal transducer and activator of transcription 3), signaling pathways (transforming growth factor‐β1, RAC‐α serine/threonine‐protein kinase, Wnt, nuclear factor‐kappa B, peroxisome proliferator‐activated receptor, Notch, and RAS), RNA‐binding proteins (ESRP1 and ESRP2) and microRNAs. Therefore, drugs targeting EMT may be a promising therapy against both fibrosis and tumors. A large number of compounds that are synthesized or derived from natural products and their derivatives suppress the EMT by targeting these mediators in fibrosis and cancer. By targeting EMT, these compounds exhibited anticancer effects in multiple cancer types, and some of them also showed antifibrotic effects. Therefore, drugs targeting EMT not only have both antifibrotic and anticancer effects but also exert effective therapeutic effects on multiorgan fibrosis and cancer, which provides effective therapy against fibrosis and cancer. Taken together, the results highlighted in this review provide new concepts for discovering new antifibrotic and antitumor drugs.

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miR-145 and miR-497 suppress TGF-β-induced epithelial–mesenchymal transition of non-small cell lung cancer by targeting MTDH

Cited by 46 publications

References 36 publications

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

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

RETRACTED ARTICLE: Silencing hsa_circ_PVT1 (circPVT1) suppresses the growth and metastasis of glioblastoma multiforme cells by up-regulation of miR-199a-5p

Small molecule inhibitors of epithelial‐mesenchymal transition for the treatment of cancer and fibrosis

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