PTEN inhibits the invasion and metastasis of gastric cancer via downregulation of FAK expression

Zhang, Lingli; Liu, Jie; Shen, Lei; Zhang, Jun; Zhou, Wei; Yu, Honggang

doi:10.1016/j.cellsig.2014.01.025

Cited by 76 publications

(76 citation statements)

References 24 publications

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“…Zheng et al (43) identified that decreased PTEN expression was significantly associated with depth of invasion, lymphatic invasion, lymph node metastasis, liver metastasis and Union Internationale Contre le Cancer staging of gastric cancer (44). Functional experiments indicated tumor suppressive functions for PTEN in cell apoptosis, cell cycle arrest, proliferation, invasion and metastasis in gastric cancer cells (25)(26)(27). Consistent with previous data, the present study confirmed the low expression of PTEN in gastric cancer tissues compared with non-tumor gastric tissuesand identified the tumor suppressive functions of PTEN during gastric cancer progression.…”

Section: Discussionmentioning

confidence: 99%

“…3A). A low expression of PTEN was previously demonstrated that in gastric cancer tissues, and PTEN expression was associated with the formation and progression of gastric cancer (24)(25)(26)(27). A luciferase reporter assay was performed to evaluate whether PTEN is a direct target gene of miR-136.…”

Section: Mir-136 Directly Targets and Regulates Pten Expression In Gamentioning

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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Section: Discussionmentioning

confidence: 99%

Section: Mir-136 Directly Targets and Regulates Pten Expression In Gamentioning

confidence: 99%

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

2018

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“…It appears to be important for the recruitment of SH2-containing proteins, including Src family kinases, Cas, paxinlin, phosphoinositide 3-kinase, phospholipase C (PLC)-c and the adapter protein Grb7 [28]. Phosphatase and tensin homolog protein inhibit gastric cancer cell growth and invasion via the down-regulation of FAK expression and suggest FAK might be participate in the PTEN/PI3 K/NF-jB signaling pathway [23]. Numerous studies proved that knockdown of FAK may have effect on the downstream of FAK-PI3 K-Akt [22] and FAK-RAS-Raf-ERK [24,28] pathways.…”

Section: Lamin B1 Dapi Mergedmentioning

confidence: 98%

“…A good understanding of basic factors and steps required for tumor detection is paramount for effective diagnosis and prognosis of cancers. FAK is ubiquitously overexpressed in a number of human malignancies [22][23][24]. In this study, we constructed plasmids containing siRNA that targeted FAK gene and transfected into Caco2 and SMMC-7721 cells.…”

Section: Depletion Of Fak Reduced Lamin B1 Expressionmentioning

confidence: 99%

The effects of focal adhesion kinase on the motility, proliferation and apoptosis of Caco2 and SMMC-7721 cells

Gao

et al. 2015

Med Oncol

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Focal adhesion kinase (FAK) plays important roles in cancer development. However, the significance of FAK expression in colorectal carcinoma and hepatocellular carcinoma has not been clarified. This study aims to explore the roles FAK played in the progression of colorectal carcinoma and hepatocellular carcinoma. RNAi method was used to inhibit the expression of FAK in Caco2 and SMMC-7721 cells. Reverse transcriptase polymerase chain reaction analysis and Western blot analysis were used to examine mRNA and protein expression of FAK. Then, the proliferation, motility and apoptosis of both types of cells were detected using MTT assay, wound healing/transwell assay and nuclear staining assay. The microstructure changes (F-actin, β-tubulin and lamin B1) of SMMC-7721 cells were visualized by immunofluorescence. FAK was overexpressed in both cell lines and down-regulation of FAK resulted in suppression of cell proliferation, inhibition of cell migration and invasion. The apoptosis of cells was increased significantly following the FAK expression inhibition. Moreover, actin polymerization, β-tubulin and lamin B1 expression of cells were significantly decreased. The results highlight the role of FAK in the progression of cancers. These findings suggest FAK serve as a potential therapeutic target for cancer therapy.

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“…In the case of the tumor suppressor PTEN, it is interesting to note that metastases often have no expression of PTEN, although the primary tumor itself expresses PTEN (6). This may indicate that cells capable of initiating metastasis originate from cellular selection (7), whereby cells with little or no expression of PTEN are more likely to initiate successful metastases (8, 9). Furthermore, it is known from a series of studies of two tumor systems that tumors “talk” to each other through serum-borne factors (10–12).…”

mentioning

confidence: 99%

The Yinâ€“Yang of Microvesicles (Exosomes) in Cancer Biology

Al‐Nedawi

2014

Front. Oncol.

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PTEN inhibits the invasion and metastasis of gastric cancer via downregulation of FAK expression

Cited by 76 publications

References 24 publications

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

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

The effects of focal adhesion kinase on the motility, proliferation and apoptosis of Caco2 and SMMC-7721 cells

The Yinâ€“Yang of Microvesicles (Exosomes) in Cancer Biology

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