miR-125b inhibited epithelialal&amp;ndash;mesenchymal transition of triple-negative breast cancer by targeting MAP2K7

Hong, Liquan; Pan, Feng; Jiang, Huifen; Zhang, Lahong; Liu, Yuhua; Cheng, Can; Chen, Hua; Luo, Xian; Sun, Jinhua; Chen, Zhaojun

doi:10.2147/ott.s102713

Cited by 28 publications

(20 citation statements)

References 31 publications

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“…Although the expression and functional role of miR-125b in different types of tumors are controversial, relevant studies show that it mostly acts as a tumor suppressor gene in solid tumors [ 32 ]. For example, miR-125b could inhibit invasion and metastasis of tumor cells, and it has been identified as a tumor suppressor gene in breast cancer [ 16 ] and bladder cancer [ 33 ]. Its expression levels in serum can be regarded as a biomarker to identify whether patients with non-small cell lung cancer could receive DDP-based chemotherapy [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

“…In gastric cancer, miR-125b overexpression may increase proliferation but decrease apoptosis [ 15 ]. However, in breast cancer, miR-125b can significantly inhibit tumor proliferation [ 16 ]. Additionally, the significant effect of miR-125b on the response to radiochemotherapy in various cancers, such as glioblastoma [ 17 ], oral squamous cell carcinoma [ 18 ] and ovarian cancer [ 19 ], has also been proved.…”

Section: Introductionmentioning

confidence: 99%

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The functional mechanism of miR-125b in gastric cancer and its effect on the chemosensitivity of cisplatin

Zhang

Yao

Guo³

et al. 2017

Oncotarget

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Numerous studies have shown drug resistance of gastric cancer cells could be modulated by abnormal expression of microRNAs. Cisplatin (DDP) is one of the most commonly used drugs for chemotherapy of gastric cancer. In this study, the potential function of miR-125b on DDP resistance in gastric cancer cells was investigated. Sixteen miRNAs significantly differential expressed in gastric tumor tissues and adjacent tissues were characterized and their corresponding putative target genes were also screened. MiR-125b was selected as our focus for its evident down-regulated expression among candidate genes. Real-time polymerase chain reaction assay indicated that miR-125b was significantly down-regulated in gastric cancer tissues and various cell lines. HER2 was identified as a target gene of miR-125b by dual luciferase reporter assay and Western blot. Moreover, miR-125b overexpression inhibited not only the proliferation, migration, and invasion abilities of HGC-27 and MGC-803 cells, but also in vivo tumor growth of MGC-803 cells by an intratumoral delivery approach. Notably, we observed up-regulated miR-125b contributed to the chemosensitivity of DDP in HGC-27 and MGC-803 cells at different concentrations and also possessed sensibilization for DDP at different times. MiR-125b expression was found to be related to lymph node metastasis, HER2 expression and overall survival of patients through correlation analysis. Collectively, these results indicate miR-125b may regulate DDP resistance as a promising therapeutic target for gastric cancer treatment in future.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The functional mechanism of miR-125b in gastric cancer and its effect on the chemosensitivity of cisplatin

Zhang

Yao

Guo³

et al. 2017

Oncotarget

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show abstract

“…Upregulation of miR-125b as an oncogene has been reported in various cancers: nasopharyngeal carcinoma (NPC), 13,14 retinoblastoma (RB), 15 glioblastoma (GBM), [16][17][18][19][20] poorly differentiated non-small-cell lung cancer (NSCLC), 21 acute lymphoblastic leukemia (ALL), 22 acute myeloid leukemia (AML), 23 and gastric cancer. [24][25][26] On the other hand, miR-125b, as a tumor suppressor, is downregulated in the following cancers: non-small-cell lung cancer (NSCLC), 27 esophageal squamous cell carcinoma (ESCC), 28,29 anaplastic thyroid cancer, 30 bladder cancer, [31][32][33][34][35] hepatocellular carcinoma (HCC), [36][37][38][39] melanoma, 40,41 ovarian cancer, [42][43][44] osteosarcoma, [45][46][47] chondrosarcoma, 48 breast cancer, [49][50][51][52][53][54][55] gallbladder cancer (GBC), 56 endometrioid endometrial cancer (EEC), 57 colorectal cancer (CRC), 58,…”

Section: Introductionmentioning

confidence: 99%

<p>The Emerging Roles of miR-125b in Cancers</p>

Wang¹,

Zeng²,

Jiang³

2020

CMAR

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MicroRNAs (miRNAs) are endogenous, noncoding, single-stranded RNA molecules of 22 nucleotides in length. MiRNAs have both tumor-suppressive properties and oncogenic properties that can control critical processes in tumors. Mature miR-125b originates from miR-125b-1 and miR-125b-2 and leads to the degradation of target mRNAs or the inhibition of translation through binding to the 3′ untranslated regions (3′-UTR) of target mRNAs. Importantly, miR-125b is involved in regulating NF-κB, p53, PI3K/Akt/mTOR, ErbB2, Wnt, and another signaling pathways, thereby controlling cell proliferation, differentiation, metabolism, apoptosis, drug resistance and tumor immunity. This review aims to summarize the recent literature on the role of miR-125b in the regulation of tumorigenesis and to explore its potential clinical application in the diagnosis, prognosis and clinical treatment of tumors.

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“…In anaplastic thyroid cancer, miR-125b-5p could inhibit the migration and invasion of tumor cells by targeting PIK3CD [ 9 ]. In triple-negative breast cancer, miR-125b-5p inhibited the epithelial-mesenchymal transition (EMT) by targeting MAP2K7 [ 10 ]. In gastric cancer, miR-125b-5p suppressed the proliferation and invasion of tumor cells by targeting MCL1 [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

miR-125b-5p functions as a tumor suppressor gene partially by regulating HMGA2 in esophageal squamous cell carcinoma

et al. 2017

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MicroRNAs (miRNAs) play important roles in the progression of human cancer including esophageal squamous cell carcinoma (ESCC). Although previous reports showed that miR-125b-5p was down-regulated in ESCC, the roles and mechanisms of loss of function of miR-125b-5p in ESCC were still unknown. Using microRNA microarray and GEO datasets, we found and confirmed that miR-125b-5p was down-regulated in ESCC tissues. In-vitro assays showed that ectopic miR-125b-5p expression repressed cell proliferation, migration and invasion, and induced cell senescence. We also found that miR-125b-5p reduced the expressions of cell cycle regulatory genes including CCNA2, CCND1 and CCNE1, and regulated the markers of epithelial to mesenchymal transition (EMT) including E-cadherin, N-cadherin and EMT associated transcription factor Slug, and also decreased the MMPs including MMP2, MMP7 and MMP13. Furthermore, the candidate target gene HMGA2 was negatively regulated by miR-125b-5p both in mRNA and protein levels. Importantly, knockdown of HMGA2 partially phenocopied the effects of miR-125b-5p overexpression on cell cycle regulators and EMT markers. In conclusion, our results suggested that overexpression of miR-125b-5p inhibited cell proliferation, migration and invasion partially by down-regulating HMGA2 in ESCC.

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miR-125b inhibited epithelialal–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7

Cited by 28 publications

References 31 publications

The functional mechanism of miR-125b in gastric cancer and its effect on the chemosensitivity of cisplatin

The functional mechanism of miR-125b in gastric cancer and its effect on the chemosensitivity of cisplatin

<p>The Emerging Roles of miR-125b in Cancers</p>

miR-125b-5p functions as a tumor suppressor gene partially by regulating HMGA2 in esophageal squamous cell carcinoma

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