Erratum to: Promyelocytic leukemia protein enhances apoptosis of gastric cancer cells through Yes-associated protein

Xu, Zhipeng; Chen, Jiamin; Shao, Liming; Ma, Wangqian; Xu, Dingting

doi:10.1007/s13277-015-4658-6

Cited by 2 publications

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“…These results indicate a relationship between the Hippo pathway and cell apoptosis, and are consistent with previous studies 37 - 40 . For example, in mouse mammary epithelial cells, overexpression of YAP suppresses TGF-β1-induced apoptosis, while knockdown of YAP induces apoptosis 37 ; in human renal carcinoma cells, curcumin enhances temsirolimus-induced apoptosis through upregulation of YAP/p53 38 ; in human pulmonary micro-vascular endothelial cells, lipopolysaccharide induces apoptosis via the YAP signaling pathway 39 ; and promyelocytic leukemia protein enhances apoptosis of gastric cancer cells through YAP 40 . Notably, the expression levels of caspase 3 and Bcl-2 family members (Bak, Bid, and Bik) decreased when YAP was overexpressed, suggesting that the Hippo pathway affects the Bcl-2 family to regulate apoptosis in h-PDLSCs.…”

Section: Discussionsupporting

confidence: 93%

Activated Yes-Associated Protein Accelerates Cell Cycle, Inhibits Apoptosis, and Delays Senescence in Human Periodontal Ligament Stem Cells

Jia¹,

Gu²,

Zhang³

et al. 2018

Int. J. Med. Sci.

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Objectives: To provide insight into the biological effects of activated Yes-associated protein (YAP) on the proliferation, apoptosis, and senescence of human periodontal ligament stem cells (h-PDLSCs).Methods: h-PDLSCs were isolated by the limiting dilution method, and their surface markers were quantified by flow cytometry. Enhanced green fluorescence protein (EGFP)-labeled lentiviral vector was used to activate YAP in h-PDLSCs, then qRT-PCR and Western blotting were used to evaluate the expression level of YAP. Immunofluorescence was used to detect the location of YAP in h-PDLSCs. The proliferation activity was detected by cell counting kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU), and the cell cycle was determined by flow cytometry. Apoptosis was analyzed by Annexin V-APC staining. Cell senescence was detected by β-galactosidase staining. Proteins in ERK, Bcl-2, and p53 signaling pathways were detected by Western blotting.Results: h-PDLSCs were isolated successfully and were positive for human mesenchymal stem cell surface markers. After YAP was activated by lentiviral vector, the mRNA and protein of YAP were highly expressed, and more YAP translocated into the nucleus. When YAP was overexpressed in h-PDLSCs, proliferation activity was improved; early and late apoptosis rates decreased (P<0.05); the proportion of cells in G2/M phases increased (P<0.05), while that in G0/G1 phase decreased (P<0.05); cellular senescence was delayed (P<0.01); the expression of P-MEK, P-ERK, P-P90RSK and P-Msk increased, while the expression of Bcl-2 family members (Bak, Bid and Bik) decreased.Conclusions: Activated YAP promotes proliferation, inhibits apoptosis, and delays senescence of h-PDLSCs. The Hippo-YAP signaling pathway can influence ERK and Bcl-2 signaling pathways.

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Section: Discussionsupporting

confidence: 93%

Activated Yes-Associated Protein Accelerates Cell Cycle, Inhibits Apoptosis, and Delays Senescence in Human Periodontal Ligament Stem Cells

Jia¹,

Gu²,

Zhang³

et al. 2018

Int. J. Med. Sci.

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Role of piwi‑interacting RNA‑651 in the carcinogenesis of non‑small cell lung cancer

et al. 2017

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Piwi-interacting RNAs (piRNAs/piRs) are small non-coding RNAs that can serve important roles in genome stability by silencing transposable genetic elements. piR651, one of these novel piRNAs, regulates a number of biological functions, as well as carcinogenesis. Previous studies have reported that piR651 is overexpressed in human gastric cancer tissues and in several cancer cell lines, including non-small cell lung cancer (NSCLC) cell lines. However, the role of piRNAs in carcinogenesis has not been clearly defined. In the present study, a small interfering RNA inhibitor of piR651 was transfected into the NSCLC A549 and HCC827 cell lines to evaluate the effect of piR651 on cell growth. The association between piR651 expression and apoptosis was evaluated by flow cytometry and western blot analysis. Wound-healing and Transwell migration and invasion assays were used to determine the effect of piR651 on the migration and invasion of NSCLC cell lines. The results revealed that inhibition of piR651 inhibited cell proliferation and significantly increased the apoptotic rate compared with the negative control (NC), as well as altering the expression of apoptosis-associated proteins. There were fewer migrating and invading cells in the piR651-inhibited group than in the NC group in the Transwell assays. Furthermore, in the wound-healing assay, the wound remained wider in the piR651 inhibitor group, suggesting decreased cell migration compared with that in the NC group. The results of the present study demonstrate that piR651 potentially regulates NSCLC tumorigenic behavior by inhibiting cell proliferation, migration and invasion and by inducing apoptosis. Therefore, piR651 is a potential cancer diagnosis marker.

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Erratum to: Promyelocytic leukemia protein enhances apoptosis of gastric cancer cells through Yes-associated protein

Cited by 2 publications

References 0 publications

Activated Yes-Associated Protein Accelerates Cell Cycle, Inhibits Apoptosis, and Delays Senescence in Human Periodontal Ligament Stem Cells

Activated Yes-Associated Protein Accelerates Cell Cycle, Inhibits Apoptosis, and Delays Senescence in Human Periodontal Ligament Stem Cells

Role of piwi‑interacting RNA‑651 in the carcinogenesis of non‑small cell lung cancer

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