Molecular and therapeutic insight into ER stress signalling in NSCLC.

Abstract\nHIGHLIGHTSEndoplasmic Reticulum (ER) stress is intricately involved in cancer development, progression and response to chemotherapy. ER stress related genes might play an important role in predicting the prognosis in lung adenocarcinoma patients and may be manipulated to improve the treatment outcome and overall survival rate. In this review, we analysed the contribution of the three major ER stress pathways—IRE1, ATF6, and PERK—in lung cancer pathogenesis <italic>via</italic> modulation of tumour microenvironment (TME) and processes as metastasis, angiogenesis, apoptosis and N-glycosylation. Furthermore, we discuss the regulatory role of microRNAs in fine-tuning ER stress pathways in Non-Small Cell Lung Cancer (NSCLC). Our review also highlights various promising strategies to overcome chemoresistance by targeting ER stress pathways, offering new therapeutic opportunities.Endoplasmic reticulum (ER) stress manifests as loss of protein homeostasis leading to accumulation of misfolded/unfolded proteins in the ER lumenIt is triggered by stimuli as hypoxia, metabolic stress, mutations and various pathological conditions as cancer.ER stress has various repercussions in lung cancer including tumour growth progression, metastasis and chemoresistance.Various miRNAs are implicated in modulation of ER stress response in lung cancer, which may be explored further for finding the new treatment approaches.Endoplasmic reticulum (ER) stress manifests as loss of protein homeostasis leading to accumulation of misfolded/unfolded proteins in the ER lumenIt is triggered by stimuli as hypoxia, metabolic stress, mutations and various pathological conditions as cancer.ER stress has various repercussions in lung cancer including tumour growth progression, metastasis and chemoresistance.Various miRNAs are implicated in modulation of ER stress response in lung cancer, which may be explored further for finding the new treatment approaches. [ABSTRACT FROM AUTHOR]