ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2017
[Clinical Significance and Mechanism of PI3K p110β Overexpression in Non-small Cell Lung Cancer].
Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- Integrative Bioinformatics Analysis Reveals Potential Target Genes and TNFα Signaling Inhibition by Brazilin in Metastatic Breast Cancer Cells.Asian Pacific journal of cancer prevention : APJCP · 2020Article
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5 authors at 2 institutions in 1 country.
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Abstract
backgroundPhosphatidylinositide 3-kinases (PI3K) pathway is one of the most important pathway in cells, which plays an important role in proliferation, growth, differentiation and mobility of cells. The aberrant activation of PI3K pathway was exsited in 50%-70% cases of non-small cell lung cancer (NSCLC). As the key point in PI3K pathway, expression of PI3K plays a critical role in activity of the pathway, which is closely related with the initiation and development of NSCLC, furthermore with the response of tumor to target treatment. Our study is to analyze the clinical significance and mechanism of PI3K p110β overexpression in NSCLC.
methodsExpression of p110β and other proteins in PI3K pathway were detected by immunohistochemistry in 170 cases of NSCLC. Correlation between expression of p110β and clinicopathological characteristics of patients as well as expression of other proteins in PI3K pathway was analyzed.
resultsIn 170 NSCLC, overexpression of p110β was found in 41.8% of cases. Correlation between overexpression of p110β and Ki 67 index was significant (P=0.040). No significant difference of p110 expression were observed among different cohorts of gender, age, smoking status, classification, grade and stage (P>0.05). Correlation between expression of p110β and other proteins in PI3K pathway was various, positively correlated with PTEN loss (P<0.001) and negatively correlated with mutant EGFR (P=0.022), while not correlated with P-Akt (Ser473), HER2, ALK, ROS1 and wild type EGFR (P>0.05).
conclusionsOverexpression of p110β is frequently detected in NSCLC. It is closely related with PTEN loss NSCLC, which shows that it plays an important role in maintaining and developing of tumors driven by PTEN loss. It initiates the proliferation of tumor cells in NSCLC without phosphorylating Akt. PIK3CB mutation is not the major cause of overexpression of p110β. Dysregulation of receptor tyrosine kinases (RTKs) doesn't show potential of increasing p110β level in cancer tissue, furthermore the expression of p110β in tumors with EGFR mutation is lower than in tumors without EGFR mutation.
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