Knockdown of heat shock protein family D member 1 (HSPD1) in lung cancer cell altered secretome profile and cancer-associated fibroblast induction
Issued Date
2024-06-01
Resource Type
ISSN
01674889
eISSN
18792596
Scopus ID
2-s2.0-85191985731
Pubmed ID
38663552
Journal Title
Biochimica et Biophysica Acta - Molecular Cell Research
Volume
1871
Issue
5
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biochimica et Biophysica Acta - Molecular Cell Research Vol.1871 No.5 (2024)
Suggested Citation
Aluksanasuwan S., Somsuan K., Ngoenkam J., Chiangjong W., Rongjumnong A., Morchang A., Chutipongtanate S., Pongcharoen S. Knockdown of heat shock protein family D member 1 (HSPD1) in lung cancer cell altered secretome profile and cancer-associated fibroblast induction. Biochimica et Biophysica Acta - Molecular Cell Research Vol.1871 No.5 (2024). doi:10.1016/j.bbamcr.2024.119736 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/98278
Title
Knockdown of heat shock protein family D member 1 (HSPD1) in lung cancer cell altered secretome profile and cancer-associated fibroblast induction
Corresponding Author(s)
Other Contributor(s)
Abstract
The crosstalk between lung cancer cells and cancer-associated fibroblast (CAF) is pivotal in cancer progression. Heat shock protein family D member 1 (HSPD1) is a potential prognostic biomarker associated with the tumor microenvironment in lung adenocarcinoma (LUAD). However, the role of HSPD1 in CAF activation remains unclear. This study established stable HSPD1-knockdown A549 lung cancer cells using a lentivirus-mediated shRNA transduction. A targeted label-free proteomic analysis identified six significantly altered secretory proteins in the shHSPD1-A549 secretome compared to shControl-A549. Functional enrichment analysis highlighted their involvement in cell-to-cell communication and immune responses within the tumor microenvironment. Additionally, most altered proteins exhibited positive correlations and significant prognostic impacts on LUAD patient survival. Investigations on the effects of lung cancer secretomes on lung fibroblast WI-38 cells revealed that the shControl-A549 secretome stimulated fibroblast proliferation, migration, and CAF marker expression. These effects were reversed upon the knockdown of HSPD1 in A549 cells. Altogether, our findings illustrate the role of HSPD1 in mediating CAF induction through secretory proteins, potentially contributing to the progression and aggressiveness of lung cancer.