2018•Unpublished venueOpen access

The Effect of PTEN on Apoptosis in NSCLC Cell Line

Aydın Demiray, Hakan Akça, Buket Er Urgancı

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Abstract

PTEN is inactivated in a subset of lung cancer; therefore, we investigated the involvement of PTEN inactivation in invasiveness of lung cancer cells. AKT at Ser473 was phosphorylated in several lung cancer cell lines with loss of PTEN expression. Therefore, we created a tetracycline inducible expression system of wild-type PTEN (PTEN-WT) as well as catalytically (PTEN-G129R) and lipid phosphatase (PTEN-G129E) inactive PTEN mutants using the PC14, lung adenocarcinoma cell lines, in which endogenous PTEN expression was not detected and AKT at Ser473 was phosphorylated by Western blot analysis. These results suggest that the PTEN gene cannot induce apoptosis alone, but apoptosis can be achieved by the suppression of other pathways. The absence of PTEN expression gives an invasive and metastatic phenotype to cancer cells, and also while staging of cancer cells that allows the transition to a further stage of cancer.

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What this paper is about

PTEN is inactivated in a subset of lung cancer; therefore, we investigated the involvement of PTEN inactivation in invasiveness of lung cancer cells. AKT at Ser473 was phosphorylated in several lung cancer cell lines with loss of PTEN expression. Therefore, we created a tetracycline inducible expression system of wild-type PTEN (PTEN-WT) as well as catalytically (PTEN-G129R) and lipid phosphatase (PTEN-G129E) inactive PTEN mutants using the PC14, lung adenocarcinoma cell lines, in which endogenous PTEN expression was not detected and AKT at Ser473 was phosphorylated by Western blot analysis. These results suggest that the PTEN gene cannot induce apoptosis alone, but apoptosis can be achieved by the suppression of other pathways. The absence of PTEN expression gives an invasive and metastatic phenotype to cancer cells, and also while staging of cancer cells that allows the transition to a further stage of cancer.

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Available abstract

PTEN is inactivated in a subset of lung cancer; therefore, we investigated the involvement of PTEN inactivation in invasiveness of lung cancer cells. AKT at Ser473 was phosphorylated in several lung cancer cell lines with loss of PTEN expression. Therefore, we created a tetracycline inducible expression system of wild-type PTEN (PTEN-WT) as well as catalytically (PTEN-G129R) and lipid phosphatase (PTEN-G129E) inactive PTEN mutants using the PC14, lung adenocarcinoma cell lines, in which endogenous PTEN expression was not detected and AKT at Ser473 was phosphorylated by Western blot analysis. These results suggest that the PTEN gene cannot induce apoptosis alone, but apoptosis can be achieved by the suppression of other pathways. The absence of PTEN expression gives an invasive and metastatic phenotype to cancer cells, and also while staging of cancer cells that allows the transition to a further stage of cancer.

Key concepts: PTEN, Cancer research, Protein kinase B, Apoptosis, Lung cancer, Phosphatase, Biology, Cancer

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