Upregulation of miR-136 in human non-small cell lung cancer cells promotes Erk1/2 activation by targeting PPP2R2A

Shen, Shuxin; Han, Yanyan; Li, Yin; Qin, Jianjun; Li, Ke; Liu, Ying; Wang, Jiaxiang

doi:10.1007/s13277-013-1087-2

Cited by 74 publications

(77 citation statements)

References 35 publications

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“…For example, in NSCLC, expression of miR-136-5p promoted cell proliferation by promoting extracellular signal-regulated kinase (ERK)1/2 phosphorylation via the targeting of protein phosphatase 2 regulatory subunit Bα (PPP2R2A) (13). This result supports the hypothesis that miR-136 acts as an oncogene in NSCLC.…”

Section: Discussionsupporting

confidence: 58%

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Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

et al. 2018

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Abstract. MicroRNAs (miRs) are involved in diverse physiological and developmental processes at the post-transcriptional level in cells. Previous studies have demonstrated that miR-136-5p is involved in certain types of cancer. However, the function of miR-136-5p in renal cell carcinoma (RCC) remains to be fully elucidated. In present study, miR-136-5p expression levels were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and MTT assays, CCK-8 assays, Transwell assays, wound healing assays and flow cytometry were performed to investigate the function of miR-136-5p in RCC. RT-qPCR revealed that the expression of miR-136 was significantly lower in RCC tissues and cells compared with adjacent non-tumor tissues and cells in vitro. miR-136-5pwas also demonstrated to be associated with RCC cell proliferation, viability, migration, invasion and apoptosis. miR-136-5p may therefore function as a tumor suppressor in RCC. Further studies are required to elucidate the molecular mechanisms and signaling pathways underlying these functions of miR-136-5p, to investigate the potential function of miR-136-5p as a biomarker for the early detection and prognosis of RCC, and its potential as a therapeutic target for the treatment of RCC.

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Section: Discussionsupporting

confidence: 58%

“…Previous studies have demonstrated that miR-136-5p is involved in a number of types of carcinoma, including (12) and non-small cell lung cancer (NSCLC) (13). However, the function of miR-136-5p in RCC remains to be explored.…”

Section: Introductionmentioning

confidence: 99%

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

et al. 2018

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“…These findings suggested that miR-136 serves tumor suppressive functions in these types of cancer. Conversely, in non-small cell lung cancer, miR-136 was up regulated and markedly associated with tumor type and differentiation (22). The downregulation of miR-136 expression repressed anchorage-dependent and anchorage-independent proliferation in non-small cell lung cancer (22).…”

Section: Discussionmentioning

confidence: 96%

“…Conversely, in non-small cell lung cancer, miR-136 was up regulated and markedly associated with tumor type and differentiation (22). The downregulation of miR-136 expression repressed anchorage-dependent and anchorage-independent proliferation in non-small cell lung cancer (22). These studies draw conflicting conclusions that miR-136 may act as an oncogene in certain types of cancer and tumor suppressor in others.…”

Section: Discussionmentioning

confidence: 99%

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Microrna-136 promotes proliferation and invasion ingastric cancer cells through Pten/Akt/P-Akt signaling pathway

2018

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Abstract. Gastric cancer is the fourth most common cancer and the second most frequent cause of cancer-associated mortality in the world. Previous studies have revealed that expression levels of microRNAs (miRNAs) are associated with the initiation and progression of several types of cancer, including gastric cancer. Previous studies have demonstrated that the abnormal expression of miRNA-136 may serve a function in the progression of several types of human cancer. However, the expression pattern of miR-136, its functions and underlying molecular mechanisms in gastric cancer remain unresolved. In the present study, it was revealed that the expression of miR-136 was aberrantly up regulated in gastric cancer tissues and cell lines. The suppression of miR-136 was able to inhibit proliferation and invasion in gastric cancer cell lines. Furthermore, phosphatase and tensin homolog (PTEN) was identified as a direct target gene of miR-136 in gastric cancer. PTEN was under expressed in gastric cancer tissues compared with non-tumor gastric tissues, and PTEN expression was negatively correlated with miR-136 expression. Furthermore, PTEN overexpression mimics the effects of miR-136 knockdown on gastric cancer cells. Additionally, miR-136 under expression decreased phospho-(p) AKT expression, but did not affect AKT expression in gastric cancer cells. In conclusion, the data of the present study suggest that miR-136 acts as an oncogene in gastric cancer via regulation of the PTEN/AKT/p-AKT signaling pathway and may potentially serve as a novel therapeutic target for the treatment of gastric cancer.

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LCK‐Mediated RIPK3 Activation Controls Double‐Positive Thymocyte Proliferation and Restrains Thymic Lymphoma by Regulating the PP2A‐ERK Axis

Hwang

Koo

et al. 2022

Advanced Science

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Receptor‐interacting protein kinase 3 (RIPK3) is the primary regulator of necroptotic cell death. RIPK3 expression is often silenced in various cancer cells, which suggests that it may have tumor suppressor properties. However, the exact mechanism by which RIPK3 negatively regulates cancer development and progression remains unclear. This report indicates that RIPK3 acts as a potent regulator of the homeostatic proliferation of CD4+CD8+ double‐positive (DP) thymocytes. Abnormal proliferation of RIPK3‐deficient DP thymocytes occurs independently of the well‐known role for RIPK3 in necroptosis (upstream of MLKL activation), and is associated with an incidental thymic mass, likely thymic hyperplasia. In addition, Ripk3‐null mice develop increased thymic tumor formation accompanied by reduced host survival in the context of an N‐ethyl‐N‐nitrosourea (ENU)‐induced tumor model. Moreover, RIPK3 deficiency in p53‐null mice promotes thymic lymphoma development via upregulated extracellular signal‐regulated kinase (ERK) signaling, which correlates with markedly reduced survival rates. Mechanistically, lymphocyte‐specific protein tyrosine kinase (LCK) activates RIPK3, which in turn leads to increases in the phosphatase activity of protein phosphatase 2 (PP2A), thereby suppressing hyper‐activation of ERK in DP thymocytes. Overall, these findings suggest that a RIPK3‐PP2A‐ERK signaling axis regulates DP thymocyte homeostasis and may provide a potential therapeutic target to improve thymic lymphoma therapies.

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Upregulation of miR-136 in human non-small cell lung cancer cells promotes Erk1/2 activation by targeting PPP2R2A

Cited by 74 publications

References 35 publications

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

Microrna-136 promotes proliferation and invasion ingastric cancer cells through Pten/Akt/P-Akt signaling pathway

LCK‐Mediated RIPK3 Activation Controls Double‐Positive Thymocyte Proliferation and Restrains Thymic Lymphoma by Regulating the PP2A‐ERK Axis

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