Endoplasmic reticulum stress pathway mediated by Grp78 may be responsible for controlling the growth of lung cancer cells

Upregulation of GRP78 and GRP94 can significantly confer the chemoresistance to VP-16 in human lung cancer cell line SK-MES-1.

Results indicated that overexpression of GRP78 can enhance the sensitivity to cisplatin and there is correlation between the expression of GRP78 and resistance to cisplatin of human lung cancer SPCA-1 cell line.

The expression levels of GRP78 and Bax were related to the carcinogenesis, development and metastasis of non-small cell lung cancer.

The expression of GRIM-1 and GRP78 was negatively correlated in human non-small cell lung cancer (NSCLC) tissues, and the down-regulation of GRP78 by GRIM-1 provides a possible mechanism for their interaction.

cancer-associated fibroblasts induced GRP78 expression in A549 and SPCA-1 cells to facilitate Non-Small Cell lung cancer cell migration and invasion

Antibodies targeting GRP78 exhibited antitumor activity and enhanced the efficacy of radiation in Non-small cell lung cancer and glioblastoma multiforme both in vitro and in vivo GRP78 is a promising novel target, and anti-GRP78 antibodies could be used as an effective cancer therapy alone or in combination with ionizing radiation

this study shows that overexpression of GRP78 predicts poor prognosis in pulmonary adenocarcinoma

expression not predictive of survival in locally advanced non-small cell lung cancer

Knockdown of OTUD3 results in a decrease in the level of GRP78 protein, suppression of cell growth and migration, and tumorigenesis in lung cancer.

GALNT6 promotes invasion and metastasis of human lung adenocarcinoma cells through O-glycosylating chaperone protein GRP78.