Predictive and Prognostic Biomarkers for Patients Treated with Anti-EGFR Agents in Lung Cancer: A Systemic Review and Meta-Analysis

Wang, Ying; Qu, Xiao; Shen, Hongchang; Wang, Kai; Liu, Qi; Du, Jiajun

doi:10.7314/apjcp.2015.16.11.4759

Cited by 6 publications

(2 citation statements)

References 71 publications

(66 reference statements)

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“…Personalized pharmacotherapy is gaining popularity in clinical oncology. Human genome sequencing has been legalized which will bring more potential therapeutic targets [2–4]. Therefore, understanding the molecular mechanisms and developing novel therapeutic targets for lung cancer are imperative.…”

Section: Introductionmentioning

confidence: 99%

Blockade efficacy of MEK/ERK-dependent autophagy enhances PI3K/Akt inhibitor NVP-BKM120's therapeutic effectiveness in lung cancer cells

et al. 2016

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NVP-BKM120 (BKM120) is a new pan-class I phosphatidylinositol-3 kinase (PI3K) inhibitor and has been tested in clinical trials as an anticancer agent. In this study, we determined whether BKM120 induces autophagy and the impact of autophagy induction on BKM120's growth-inhibitory activity. BKM120 potently induced elevation of autophagosome-bound type II LC3 (LC3-II) protein, predominantly in cell lines insensitive to BKM120, thereby inducing autophagy. The presence of lysosomal protease inhibitor chloroquine further enhanced the levels of LC3-II. BKM120 combined with chloroquine, enhanced growth-inhibitory effects including induction of apoptosis, suggesting that autophagy is a protective mechanism counteracting BKM120's growth-inhibitory activity. Interestingly, BKM120 increased p-ERK1/2 levels. When blocking the activation of this signaling with MEK inhibitors or with knockdown of ERK1/2, the ability of BKM120 to increase LC3-II was attenuated and the growth-inhibitory effects including induction of apoptosis were accordingly enhanced, suggesting that the MEK/ERK activation contributes to BKM120-induced authophagy. In mouse xenograft model, we also found that the combination of BKM120 and PD0325901 synergistically suppressed cell growth in human lung cancer cells. Thus, the current study not only reveals mechanisms accounting for BKM120-induced autophagy, but also suggests an alternative method to enhance BKM120's therapeutic efficacy against non-small cell lung cancer(NSCLC) by blocking autophagy with either a lysosomal protease inhibitor or MEK inhibitor.

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Section: Introductionmentioning

confidence: 99%

Blockade efficacy of MEK/ERK-dependent autophagy enhances PI3K/Akt inhibitor NVP-BKM120's therapeutic effectiveness in lung cancer cells

et al. 2016

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show abstract

“…Personalized pharmacotherapy is gaining popularity in clinical oncology. Human genome sequencing has been legalized which will bring more potential therapeutic targets [2][3][4]. Therefore, understanding the molecular mechanisms and developing novel therapeutic targets for lung cancer are imperative.…”

Section: Introductionmentioning

confidence: 99%

Blockade Efficacy of MEK/ERK-Dependent Autophagy Enhances PI3K/Akt Inhibitor NVP-BKM120's Therapeutic Effectiveness in Lung Cancer Cells

Ren

Chen

2016

Chest

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Co-targeting PI3K/Akt and MAPK/ERK pathways leads to an enhanced antitumor effect on human hypopharyngeal squamous cell carcinoma

Peng

Liu

Zhu

et al. 2019

J Cancer Res Clin Oncol

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Predictive and Prognostic Biomarkers for Patients Treated with Anti-EGFR Agents in Lung Cancer: A Systemic Review and Meta-Analysis

Cited by 6 publications

References 71 publications

Blockade efficacy of MEK/ERK-dependent autophagy enhances PI3K/Akt inhibitor NVP-BKM120's therapeutic effectiveness in lung cancer cells

Blockade efficacy of MEK/ERK-dependent autophagy enhances PI3K/Akt inhibitor NVP-BKM120's therapeutic effectiveness in lung cancer cells

Blockade Efficacy of MEK/ERK-Dependent Autophagy Enhances PI3K/Akt Inhibitor NVP-BKM120's Therapeutic Effectiveness in Lung Cancer Cells

Co-targeting PI3K/Akt and MAPK/ERK pathways leads to an enhanced antitumor effect on human hypopharyngeal squamous cell carcinoma

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