miR-375 Inhibits Proliferation of Mouse Pancreatic Progenitor Cells by Targeting YAP1

Zhang, Zhenwu; Men, Tong; Feng, Rui-cheng; Li, Yunchao; Zhou, Di; Teng, Chun‐Bo

doi:10.1159/000356614

Cited by 60 publications

(51 citation statements)

References 38 publications

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“…miR-375 was primary identified in the human pancreas in 2004 (36), and Avnit-Sagi et al (37) suggested that miR-375 was expressed at a very high level in human pancreatic islets and brain tissue. Previous studies also identified that miR-375 was involved in numerous types of cancer (38)(39)(40): The expression of miR-375 was downregulated in human gastric cancer cells, and the induction of miR-375 expression may affect the biological function of cells (41); Zhang et al (42) also identified that miR-375 expression was abnormally regulated in pancreatic progenitor cells, and that the regulation of miR-375 expression may inhibit cell proliferation through targeting Yes associated protein 1. However, the biological effect of miR-375 in human liver cancer has not been fully studied.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of miR‑375 inhibits human liver cancer cell growth by modulating cell proliferation and apoptosis via targeting ErbB2

Jia

Ding

2018

Oncol Lett

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Abstract. microRNAs (miRNA/miRs) are a class of small non-coding RNAs; they serve important biological roles in tumorigenesis through the regulation of oncogene expression, and they may be used for the diagnosis and treatment of human cancer. miR-375 was identified to exhibit abnormal expression levels in a number of types of tumor; however, the biological role of miR-375 in human hepatocellular carcinoma (HCC) remains incompletely characterized. The present study investigated the expression of miR-375 in human HCC tissues and human liver cancer cell lines; results from a reverse transcription quantitative polymerase chain reaction analysis indicated that the expression of miR-375 was significantly decreased in tissues and live cancer cell lines, compared with normal tissues and PHH cells. Additional studies demonstrated that the upregulation of miR-375 inhibited human liver cancer cell growth via regulation of cell apoptosis. It was also revealed that the receptor tyrosine-protein kinase erbB-2 (ErbB2) gene was a direct target gene of miR-375, and that the regulation of ErbB2 was associated with the human liver cancer growth. Therefore, the present study demonstrated that miR-375 was expressed at low levels both in human HCC tissues and cell line, compared with normal tissues and PHH cells, and that the induction of miR-375 expression may regulate human liver cancer cell function through targeting the ErbB2 gene, which may potentially improve the diagnosis and treatment of patients with HCC in the future.

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Section: Discussionmentioning

confidence: 99%

Upregulation of miR‑375 inhibits human liver cancer cell growth by modulating cell proliferation and apoptosis via targeting ErbB2

Jia

Ding

2018

Oncol Lett

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“…Recent evidence suggests that the Hippo-YAP pathway provides a new method for cancer treatment in clinical studies [37, 38]. However, the application of this signaling pathway to the treatment of ovarian diseases has not been tested.…”

Section: Discussionmentioning

confidence: 99%

The Hippo Signaling Pathway Regulates Ovarian Function via the Proliferation of Ovarian Germline Stem Cells

Zheng

et al. 2017

Cell Physiol Biochem

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Objective: To improve the separation, identification and cultivation of ovarian germline stem cells (OGSCs), to clarify the relationship between the Hippo signaling pathway effector YAP1 and the proliferation and differentiation of OGSCs in vitro and to identify the major contribution of Hippo signaling to ovarian function. Methods: Two-step enzymatic separation processes and magnetic separation were used to isolate and identify OGSCs by determining the expression of Mvh, Oct4, Nanog, Fragilis and Stella markers. Then, YAP1, as the main effector molecule in the Hippo signaling pathway, was chosen as the target gene of the study. Lentivirus containing overexpressed YAP1 or a YAP1-targeted shRNA was transduced into OGSCs. The effects of modulating the Hippo signaling pathway on the proliferation, differentiation, reproduction and endocrine function of ovaries were observed by microinjecting the lentiviral vectors with overexpressed YAP1 or YAP1 shRNA into infertile mouse models or natural mice of reproductive age. Results: (1) The specific expression of Mvh, Oct4, Nanog, Fragilis and Stella markers was observed in isolated stem cells. Thus, the isolated cells were preliminarily identified as OGSCs. (2) The co-expression of LATS2, MST1, YAP1 and MVH was observed in isolated OGSCs. Mvh and Oct4 expression levels were significantly increased in OGSCs overexpressing YAP1 compared to GFP controls. Consistently, Mvh and Oct4 levels were significantly decreased in cells expressing YAP1-targeted shRNA. (3) After 14-75 days of YAP1 overexpression in infertile mouse models, we detected follicle regeneration in ovaries, the activation of primordial follicles and increased birth rate, accompanied by increasing levels of E2 and FSH. (4) However, we detected decreasing follicles in ovaries, lower birth rate, and decreasing E2 and FSH in serum from healthy mice of reproductive age following YAP1 shRNA expression. Conclusion: Methods for the isolation, identification and culture of OGSCs were successfully established. Further results indicate that isolated OGSCs can specifically recognize Hippo signaling molecules and that manipulation of YAP1 expression can be used to regulate the proliferation and differentiation of OGSCs, as well as ovarian function in mice. This study suggests that the Hippo signaling pathway may represent a new molecular target for the regulation of mouse ovarian functional remodeling.

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“…As major downstream effectors, TEAD and its coactivator YAP play a crucial role in the expansion of pancreatic progenitors by controlling key pancreatic signaling mediators and transcription factors in the embryonic phase of pancreas development (27). Consistently, YAP depletion is sufficient to block pancreatic progenitor cell proliferation (30). However, convincing studies have revealed that YAP is not expressed in terminally differentiated mature primary human and mouse β cells.…”

Section: Introductionmentioning

confidence: 99%

Proproliferative and antiapoptotic action of exogenously introduced YAP in pancreatic β cells

Yuan¹,

Rafizadeh²,

Azizi³

et al. 2016

JCI Insight

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miR-375 Inhibits Proliferation of Mouse Pancreatic Progenitor Cells by Targeting YAP1

Cited by 60 publications

References 38 publications

Upregulation of miR‑375 inhibits human liver cancer cell growth by modulating cell proliferation and apoptosis via targeting ErbB2

Upregulation of miR‑375 inhibits human liver cancer cell growth by modulating cell proliferation and apoptosis via targeting ErbB2

The Hippo Signaling Pathway Regulates Ovarian Function via the Proliferation of Ovarian Germline Stem Cells

Proproliferative and antiapoptotic action of exogenously introduced YAP in pancreatic β cells

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