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

Chen, Xuyan; Huang, Zhiming; Chen, Renpin

doi:10.3892/ol.2018.7848

Cited by 21 publications

(27 citation statements)

References 41 publications

(45 reference statements)

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“…Furthermore, ectopic expression of miR-221 and miR-222 in GC cells led to a decreased expression level of PTEN (64). The silenced expression of PTEN in GC may additionally be due to other miRNAs negatively regulating it, including miR-136, miR-214 and miR-28 (5,12,65). Furthermore, the downregulated PTEN expression level was associated with adverse clinical parameters, including lymph node metastasis, poor differentiation and advanced TNM stage of patients with GC (65)(66)(67).…”

Section: Regulation Of Mirnas On the Pten/pi3k/akt Pathway In Gcmentioning

confidence: 99%

“…PTEN is a dual lipid and protein phosphatase and a common tumor suppressor. Since its identification, the mutational and epigenetic silencing of PTEN have been documented in various cancer types, owing to its extensive function in critical cellular processes, which may be generally divided into two categories, cell growth/survival and cell migration/adhesion, regulated through its lipid and protein phosphatase activities, respectively (12,13). The primary substrate of PTEN is PIP3, the product of PI3Ks, a lipid kinase family with the typical ability to phosphorylate the 3'-OH group in inositol phospholipids on the cell membrane (35).…”

Section: Pten/pi3k/akt Pathway In Gcmentioning

confidence: 99%

“…The phosphatase and tensin homolog (PTEN)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway represents a crucial one (11,12). PTEN, a dual protein and lipid phosphatase, primarily dephosphorylates phosphatidylinositol-3,4,5-trisphosphate (PIP3), which is the product of PI3K and is able to recruit Akt to the membrane, where it is phosphorylated and stimulated by other kinases dependent on PIP3 (13).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNAs and the PTEN/PI3K/Akt pathway in gastric cancer (Review)

Zhu

Xiong

et al. 2019

Oncol Rep

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Gastric carcinogenesis arises from complicated interactions among host, environmental and bacterial factors, which cause genetic and epigenetic dysregulation of oncogenic and tumor-suppressive genes. MicroRNAs (miRNAs), a class of small non-coding RNAs that post-transcriptionally regulate ~30% human genes, may serve as oncogenes or tumor-suppressors in malignancies, including gastric cancer (GC). Although miRNA dysregulation commonly exists in GC, exact roles miRNAs serve in the pathogenesis and promotion of this tumor remain undetermined. Recently, results of previous studies regarding mechanisms underlying miRNAs generally converged on pathways critical in cellular processes, including cell proliferation, apoptosis and invasion, among which phosphatase and tensin homolog (PTEN)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling is a fundamental one, with frequent oncogenic alterations in GC. Therefore, in the present review, the disorder and function of miRNAs and PTEN/PI3K/Akt signaling in GC are discussed. Additionally, how miRNAs transduce their effects by regulating this pathway, particularly in GC stem cells and the tumor microenvironment, and two novel hypotheses significant in carcinogenesis, tumor progression and recurrence, are discussed. Furthermore, the roles of miRNAs and the PTEN/PI3K/Akt pathway in target therapies against this lethal disease are outlined.

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Section: Regulation Of Mirnas On the Pten/pi3k/akt Pathway In Gcmentioning

confidence: 99%

Section: Pten/pi3k/akt Pathway In Gcmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNAs and the PTEN/PI3K/Akt pathway in gastric cancer (Review)

Zhu

Xiong

et al. 2019

Oncol Rep

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“…Some of the biomarkers we identified herein, including hsa-mir-22, hsa-mir-100, hsa-mir-136, hsa-mir-193b, hsa-mir-1304, NRP1, DUSP1, and MAP7D2 (cg02223323), have previously been reported in GC ( Grandclement and Borg, 2011 ; Chen et al, 2014 ; Mu et al, 2014 ; Zuo et al, 2015 ; Zheng et al, 2017 ; Chen et al, 2018 ; Kurata and Lin, 2018 ; Liu K.T. et al, 2018 ; Song et al, 2018 ; Teng et al, 2018 ; Liu et al, 2019 ; Pan et al, 2019 ; Wang et al, 2019 ).…”

Section: Discussionmentioning

confidence: 59%

Genomics Score Based on Genome-Wide Network Analysis for Prediction of Survival in Gastric Cancer: A Novel Prognostic Signature

et al. 2020

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Purpose Gastric cancer (GC) is a product of multiple genetic abnormalities, including genetic and epigenetic modifications. This study aimed to integrate various biomolecules, such as miRNAs, mRNA, and DNA methylation, into a genome-wide network and develop a nomogram for predicting the overall survival (OS) of GC. Materials and Methods A total of 329 GC cases, as a training cohort with a random of 150 examples included as a validation cohort, were screened from The Cancer Genome Atlas database. A genome-wide network was constructed based on a combination of univariate Cox regression and least absolute shrinkage and selection operator analyses, and a nomogram was established to predict 1-, 3-, and 5-year OS in the training cohort. The nomogram was then assessed in terms of calibration, discrimination, and clinical usefulness in the validation cohort. Afterward, in order to confirm the superiority of the whole gene network model and further reduce the biomarkers for the improvement of clinical usefulness, we also constructed eight other models according to the different combinations of miRNAs, mRNA, and DNA methylation sites and made corresponding comparisons. Finally, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were also performed to describe the function of this genome-wide network. Results A multivariate analysis revealed a novel prognostic factor, a genomics score (GS) comprising seven miRNAs, eight mRNA, and 19 DNA methylation sites. In the validation cohort, comparing to patients with low GS, high-GS patients (HR, 12.886; P < 0.001) were significantly associated with increased all-cause mortality. Furthermore, after stratification of the TNM stage (I, II, III, and IV), there were significant differences revealed in the survival rates between the high-GS and low-GS groups as well ( P < 0.001). The 1-, 3-, and 5-year C-index of whole genomics-based nomogram were 0.868, 0.895, and 0.928, respectively. The other models have comparable or relatively poor comprehensive performance, while they had fewer biomarkers. Besides that, DAVID 6.8 further revealed multiple molecules and pathways related to the genome-wide network, such as cytomembranes, cell cycle, and adipocytokine signaling. Conclusion We successfully developed a GS based on genome-wide network, which may represent a novel prognostic factor for GC. A combination of GS and TNM staging provides additional precision in stratifying patients with different OS prognoses, constituting a more comprehensive sub-typing system. This could potentially play an important role in future clinical practice.

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“…Previous studies have demonstrated that the PI3K/Akt signaling pathway is involved in multiple biological processes and that PTEN functions as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway, which reduces cell growth and increases cell apoptosis (18,19). miRNAs, including miR-136, miR-181a and miR-221/222, have been reported to regulate the expression of PTEN (20)(21)(22). However, the role of miR-21 with regard to the expres sion of PTEN in OSCC is not well established.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR‑21 promotes cell apoptosis in oral squamous cell carcinoma by upregulating PTEN

et al. 2018

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MicroRNA‑21 (miR‑21) has been identified as an oncogene and confirmed to serve an important role in carcinogenesis in various types of cancer. However, the effect and mechanism of miR‑21 in oral squamous cell carcinoma (OSCC) has not been fully elucidated. In the present study, miR‑21 inhibitor and empty vector were transfected into OSCC cells, and non‑transfected cells were used as a blank control. The results indicated that when compared with the control and scramble groups, miR‑21 inhibitor suppressed the expression of miR‑21. Conversely, phosphatase and tensin homolog deletion on chromosome 10 (PTEN) was markedly upregulated, and a dual luciferase reporter assay revealed PTEN to be a target gene of miR‑21. Furthermore, miR‑21 inhibitor decreased the proliferation and invasion and enhanced the apoptosis of OSCC cells. There was no significant difference in cell proliferation, invasion and apoptosis between the control and scramble groups. The present data suggested that there may be a regulatory loop between miR‑21 and PTEN, and that miR‑21 inhibition affected the proliferative, invasive and apoptotic abilities of OSCC cells. These findings indicate that miR‑21 may be a possible novel target in the treatment of OSCC.

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

Cited by 21 publications

References 41 publications

MicroRNAs and the PTEN/PI3K/Akt pathway in gastric cancer (Review)

MicroRNAs and the PTEN/PI3K/Akt pathway in gastric cancer (Review)

Genomics Score Based on Genome-Wide Network Analysis for Prediction of Survival in Gastric Cancer: A Novel Prognostic Signature

Inhibition of miR‑21 promotes cell apoptosis in oral squamous cell carcinoma by upregulating PTEN

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