The loss of MiR-139-5p promotes colitis-associated tumorigenesis by mediating PI3K/AKT/Wnt signaling

Maoa, Rurong; Zou, Fangyuan; Yang, Liyan; Lin, Shengchao; Li, Yueqi; Ma, Mingxing; Yin, Peihao; Liang, Xin; Liu, Jianwen

doi:10.1016/j.biocel.2015.10.008

Cited by 34 publications

(34 citation statements)

References 47 publications

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“…LPA4 can induce cell adhesion and aggregation through N‐cadherin and is the first LPAR found to activate Gαs activity, promoting intracellular cAMP accumulation . Besides, miRs exerted influence on inflammatory diseases and tumorigenesis, and overexpression of miR‐139‐5p suppressed the crosstalk between PI3K/AKT and Wnt pathway in colitis‐associated cancer . The PI3K/AKT signaling pathway was associated with the release of pro‐inflammatory cytokines and played a pivotal part in the development of ulcerative colitis .…”

Section: Discussionmentioning

confidence: 99%

“…32 Besides, miRs exerted influence on inflammatory diseases and tumorigenesis, and overexpression of miR-139-5p suppressed the crosstalk between PI3K/AKT and Wnt pathway in colitis-associated cancer. 18 The PI3K/AKT signaling pathway was associated with the release of proinflammatory cytokines and played a pivotal part in the development of ulcerative colitis. 36 The inhibition of miR- 127-5p is reported to promote chondrocyte proliferation and the protein levels of osteopontin, p-PI3K and p-Akt in osteoarthritis.…”

Section: Discussionmentioning

confidence: 99%

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Retracted: Microrna‐139‐5p inhibits epithelial‐mesenchymal transition and fibrosis in post‐menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway

Jiang

Tong

Fang

et al. 2018

J of Cellular Biochemistry

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The study explores whether miR-139-5p targeting LPAR4 affects epithelial-mesenchymal transition (EMT) and fibrosis in post-menopausal women with interstitial cystitis (IC) via the PI3K/Akt signaling pathway. Bladder tissues of IC and normal bladder tissues were collected. The pathology of bladder tissues was observed by HE, Masson and Picrosirius red staining. LPAR4 positive expression rate were determined by IHC. ELISA was performed to detect the levels of IL-6, IL-8, IL-10, and TNF-α. Rat IC models were randomized into seven different groups. miR-139-5p, LPAR1, LPAR2, LPAR3, LPAR4, LPAR5, P13K, Akt, E-cadherin, N-cadherin, Vimentin, TGF-β1, and CTGF expression were determined by RT-qPCR and Western blotting. Dual luciferase reporter gene assay verified that LPAR4 is a target gene of miR-139-5p. Fibrosis was a pathological manifestation of IC. The IC group showed higher LPAR4, PI3K, Akt, p-PI3K, p-Akt, N-cadherin, Vimentin, TGF-β1, and CTGF expression but lower miR-139-5p and E-cadherin expression than the normal group. The levels of IL-6, IL-8, IL-10, and TNF-α expression decreased while HB-EGF increased in the IC group in comparison of the normal group. Compared with the blank and NC groups, E-cadherin expression was increased in the miR-139-5p mimic and siRNA-LPAR4 groups, while LPAR4, PI3K, Akt, p-P13K, p-Akt, N-cadherin, Vimentin, TGF-β1, and CTGF expression were decreased. An opposite trend was found in the miR-139-5p inhibitor group. The miR-139-5p decreased in the miR-139-5p inhibitor + siRNA-LPAR4 and miR-139-5p inhibitor + wortmannin groups. Conclusively, miR-139-5p targeting LPAR4 inhibits EMT and fibrosis in post-menopausal IC women through the PI3K/Akt signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Retracted: Microrna‐139‐5p inhibits epithelial‐mesenchymal transition and fibrosis in post‐menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway

Jiang

Tong

Fang

et al. 2018

J of Cellular Biochemistry

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“…miR‐21 and members of the miR‐17‐92 cluster) or down‐regulation of microRNAs with reported oncosuppressive effects in various settings. The latter included miR‐218 , miR‐124 , miR‐487b and miR‐139‐5p .…”

Section: Resultsmentioning

confidence: 99%

The miR‐139‐5p regulates proliferation of supratentorial paediatric low‐grade gliomas by targeting the PI3K/AKT/mTORC1 signalling

Catanzaro

Besharat

Miele

et al. 2018

Neuropathology Appl Neurobio

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“…Another study confirmed that IGF-1 is able to participate in the regulation of PPARγ and c/EBP, so IGF-1 serves a crucial function in preadipocyte growth in addition to differentiation (32). Furthermore, Maoa et al (33) revealed that the deletion of miR-139-5p promoted the occurrence and development of colute carrier family 25 member 20 through the PI3K/AKT and Wnt pathway mediated by IGF-1R. Based on these and the present experimental results, the present study examined whether miR-139-5p may affect the adipogenesis of HemSCs through the IGF-1/IGF-1R pathway.…”

Section: Discussionmentioning

confidence: 75%

miR‑139‑5p affects cell proliferation, migration and adipogenesis by targeting insulin‑like growth factor 1 receptor in hemangioma stem cells

Xie

Wang

et al. 2019

Int J Mol Med

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Infant hemangioma is the most common benign tumor in infancy. The pathological development process of this tumor is separated into the proliferation period, the involution period and the composite period in which a few residual capillary-like vessels grow through the loose fibrofatty tissue. Previous studies have confirmed that insulin-like growth factor 1 (IGF-1) is able to facilitate the cell proliferation of hemangioma stem cells (HemScs) and the differentiation of HemSCs into adipocytes. Additionally, studies have confirmed that microRNAs (miRs) may serve a crucial function in regulating the IGF-1 receptor (IGF-1R). miR-139-5p often functions as a tumor suppressor. The present study was designed to investigate the mechanism of miR-139-5p in HemScs. dual luciferase reporter results verified that IGF-1R is the target gene of miR-139-5p. miR-139-5p overexpression reduced IGF-1R expression, and miR-139-5p inhibition increased IGF-1R expression. cell counting Kit-8 and Transwell migration assays demonstrated that miR-139-5p overexpression may target IGF-1R to inhibit the proliferation in addition to the migration of HemScs. Reverse transcription-quantitative PCR, oil red o staining and western blot analysis confirmed that miR-139-5p overexpression was able to reduce adipogenesis in HemScs via the IGF-1/IGF-1R pathway. In contrary, miR-139-5p inhibition substantially enhanced the proliferation, migration and adipogenesis of HemScs. Overall, miR-139-5p is able to affect the IGF-1/IGF-1R pathway by regulating IGF-1R expression, which ultimately affects the proliferation, migration and adipogenesis of HemScs.

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The loss of MiR-139-5p promotes colitis-associated tumorigenesis by mediating PI3K/AKT/Wnt signaling

Cited by 34 publications

References 47 publications

Retracted: Microrna‐139‐5p inhibits epithelial‐mesenchymal transition and fibrosis in post‐menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway

Retracted: Microrna‐139‐5p inhibits epithelial‐mesenchymal transition and fibrosis in post‐menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway

The miR‐139‐5p regulates proliferation of supratentorial paediatric low‐grade gliomas by targeting the PI3K/AKT/mTORC1 signalling

miR‑139‑5p affects cell proliferation, migration and adipogenesis by targeting insulin‑like growth factor 1 receptor in hemangioma stem cells

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