miR-202 inhibits the progression of human cervical cancer through inhibition of cyclin D1

Yi, Yuexiong; Li, Huirong; Lv, Qiongying; Wu, Kejia; Zhang, Wenfen; Zhang, Juan; Zhu, Dingjun; Liu, Qing; Zhang, Wei

doi:10.18632/oncotarget.12499

Cited by 32 publications

(30 citation statements)

References 28 publications

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“…In addition, miR-202 is decreased in the peripheral blood of oesophageal squamous cell carcinoma patients and significantly associated with the development, invasion and metastasis of oesophageal squamous cell carcinoma (37). Moreover, low expression levels of miR-202 are observed in multiple myeloma (24), colorectal cancer (22), hepatocellular carcinoma (25), lung (38) and cervical cancer (39). The high frequency of miR-202 downregulation in these types of human types of cancer suggests that miR-202 could be a diagnostic and prognostic marker for specific cancers.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-202 inhibits cell proliferation, migration and invasion of glioma by directly targeting metadherin

et al. 2017

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Glioma is the most common and aggressive type of primary malignant brain tumour. Increasing evidence has revealed that microRNAs play important roles in multiple biological processes related to glioma occurrence, development, diagnosis, treatment and prognosis. MicroRNA-202 (miR-202) has been studied in several types of human cancer, whereas the biological roles of miR-202 in glioma remain unknown. The present study, aimed to investigate the expression, clinical significance and biological roles of miR-202 in glioma, as well as its underlying molecular mechanism. We found that miR-202 was significantly downregulated in glioma tissues and cell lines. Low miR-202 expression was associated with Karnofsky performance status (KPS) score and World Health Organization (WHO) grade of glioma patients. Functional assays revealed that ectopic expression of miR-202 inhibited cell proliferation, migration and invasion of glioma. In addition, metadherin (MTDH) was identified as a direct target gene of miR-202 in glioma through bioinformatic analysis, luciferase reporter assay, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. Furthermore, MTDH expression was upregulated and negatively correlated with miR-202 expression in clinical glioma tissues. MTDH knockdown had similar roles to miR-202 overexpression in glioma cells. Rescue experiments revealed that upregulation of MTDH reversed the suppression of glioma cell growth and metastasis by miR-202. Moreover, miR-202 impaired the PI3K/Akt and Wnt/β-catenin pathways. These results highlight the tumour-suppressive effect of miR-202 in glioma, thereby suggesting that miR-202 may be a potential therapeutic target for the treatment of patients with this malignancy.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-202 inhibits cell proliferation, migration and invasion of glioma by directly targeting metadherin

et al. 2017

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“…Among these cancer-related miRNAs, miR-202 is reported to function as a tumor suppressor as well as to suppress cell proliferation, tumor progression, and drug resistance in several cancers. Cancers in which miR-202 is reported to have these effects include cervical cancer, hepatocellular carcinoma, colorectal carcinoma, multiple myeloma, and NSCLC [32][33][34][35][36]. Therefore, increasing the expression level of miR-202 in cancer cells may be considered as a novel strategy for cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

miR-202 Enhances the Anti-Tumor Effect of Cisplatin on Non-Small Cell Lung Cancer by Targeting the Ras/MAPK Pathway

Sun¹,

Wei²,

Tian³

et al. 2018

Cell Physiol Biochem

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Background/Aims: KRas is usually mutated in non-small cell lung cancer (NSCLC). The mutated KRas gene is a negative prognostic indicator that promotes tumor proliferation, metastasis, and drug resistance in NSCLC, and thus has become a target for cancer therapy. This study is focused on the effects of the microRNA (miR)-202/KRas axis in regulating chemosensitivity in NSCLC. Methods: Quantitative reverse transcriptase real-time PCR analysis was performed to examine the expression of miR-202. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays were performed to evaluate the sensitivity of cisplatin against NSCLC cells. The miR-202/KRas axis was confirmed by western blot and luciferase reporter assays. Cell apoptosis was measured by flow cytometry. KRas expression, MEK1/2 and ERK1/2 phosphorylation, and activation of caspase-9 and caspase-3 were detected by western blot. Results: A significant decrease in miR-202 expression was observed in NSCLC cells both in vivo and in vitro. In addition, miR-202 expression was associated with drug resistance. Recovery of miR-202 expression levels was found to increase the sensitivity of both NCI-H441 and A549 NSCLC cells to cisplatin treatment. Mechanically, as the Ras/mitogen-activated protein kinase (MAPK) pathway was aberrantly activated in NCI-H441 and A549 NSCLC cells, the overexpression of miR-202 was found to inhibit the Ras/MAPK pathway by targeting the KRas gene. As a result, increased miR-202 expression expanded apoptosis signaling induced by cisplatin in NSCLC cells. Conclusion: The miR-202/KRas axis controlled the chemosensitivity of NSCLC by mediating the Ras/MAPK pathway. Thus, the combination of platinum-based drugs with miR-202 may represent a novel strategy to enhance the anti-tumor effect against NSCLC.

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“…In human ESCCs, miR-202 regulated apoptosis by targeting HSF2 via mechanism involving caspase-3. A study also identified that miR-202 plays an important role in regulating cell proliferation, migration and invasion of cervical cancer (CC) by directly targeting cyclin D1, and miR-202 may represent a potential therapeutic target for patients with CC (16)(17)(18)(19)(20)(21)(22). In addition, a previous study showed that an increased serum concentration of miR-202 may be a strong independent prognostic factor for breast cancer patients (20).…”

Section: Discussionmentioning

confidence: 99%

miR‑202 acts as a potential tumor suppressor in breast cancer

et al. 2018

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Abstract. Breast cancer affects ~10% of women worldwide and is responsible for ~12% of all cancer-associated mortalities. Breast cancer is more prone to metastasis compared with other types of cancer. Up to 5% of patients with breast cancer present with incurable metastasis and an additional 10-15% of patients develop metastases within 3 years of their initial diagnosis. MicroRNAs (miRNAs) are short RNAs, 21-25 nucleotides in length, that have been shown to significantly affect gene expression. In total >2,000 miRNAs have been identified and specific miRNAs have been revealed to be associated with cancer. In the present study, we observed that the majority of breast cancer specimens collected expressed low levels of miR-202 compared with adjacent tissues and normal cell lines. Mechanistic investigations identified KRAS as a potential target gene of miR-202 and it was demonstrated that miR-202 exerted its tumor-suppressive effects by regulating the expression of KRAS in breast cancer cells. Functional assays revealed that miR-202 significantly reduced cell proliferation, migration and invasion in vitro. In summary, these results indicate the function of miR-202 in breast cancer progression and suggest that its use within breast cancer therapy is promising. IntroductionBreast cancer is one of the most common malignant tumors in women. In many areas, breast cancer is the most common malignancy in females. In China, the incidence of breast cancer is increasing annually. Because the development and progression of breast cancer are complex processes involving many genes, the underlying mechanism of breast cancer remains unclear (1,2).Single-stranded RNAs consisting of 19 to 25 nucleotides are known as microRNAs (miRNAs). These RNAs are regulatory molecules that modulate the expression of functional genes, play an important role in many biological processes, and are expressed in a tissue-and time-specific manner. miRNAs regulate gene expression at the post-transcriptional level mainly via completely complementary or partially complementary binding to the 3' UTR of the target gene, resulting in degradation or translational repression of the target gene (2-4). Studies have shown that a variety of miRNAs are involved in malignant transformation processes, such as malignant proliferation, metastasis and recurrence, and apoptosis inhibition. Studies have reported that miRNA inhibitors can reduce the high miR-21 expression in breast cancer cells, inhibiting proliferation and migration; that miR-373 can promote the metastasis of breast cancer cells; that miR-520 plays a role in promoting the development of breast cancer; and that miR-126 and miR-335 are able to inhibit breast cancer to a certain extent (5-7). Recent studies have demonstrated that miR-202 is associated with several types of cancer, miR-202 has a lower expression in several of cancers, and however, the expression and function of miR-202 have not been investigated in breast cancer (8).KRAS belongs to the RAS family; it is located on the short arm of chromosome 1...

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miR-202 inhibits the progression of human cervical cancer through inhibition of cyclin D1

Abstract: ABSTRACT

Cited by 32 publications

References 28 publications

MicroRNA-202 inhibits cell proliferation, migration and invasion of glioma by directly targeting metadherin

MicroRNA-202 inhibits cell proliferation, migration and invasion of glioma by directly targeting metadherin

miR-202 Enhances the Anti-Tumor Effect of Cisplatin on Non-Small Cell Lung Cancer by Targeting the Ras/MAPK Pathway

miR‑202 acts as a potential tumor suppressor in breast cancer

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