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Published on: July 21, 2018
Downregulation of KHSRP enhances carboplatin sensitivity in non-small cell lung cancer
Bao Wen1,2, Shuguang Bao1, Yanqing Gao1
1Department of Thoracic Tumor Surgery, Peking University Cancer Hospital (Inner Mongolia Campus) & Affiliated Cancer Hospital of Inner Mongolia Medical University, No. 42 Zhao Wu Da Road, Huhhot, 010020, Inner Mongolia Autonomous Region, China.
Background:
Carboplatin resistance represents a critical therapeutic challenge in non-small cell lung cancer (NSCLC) treatment. Although KHSRP has been implicated in lung cancer progression, its molecular mechanisms and impacts on chemotherapy sensitivity remain elusive. Notably, KHSRP has the capacity to activate the transcription of HMGB1, an oncogene known to influence chemotherapy sensitivity. However, it remains to be determined whether KHSRP affects chemotherapy response in NSCLC via HMGB1.
Methods:
KHSRP expression in NSCLC cells was analyzed using qRT-PCR. Cell proliferation, apoptosis, and migration were evaluated using colony formation, flow cytometry and wound healing assays. A luciferase reporter assay was conducted to assess whether KHSRP transcriptionally regulates HMGB1. Additionally, A549 cell xenografts were established in nude mice to investigate the tumor growth-promoting effects of KHSRP in vivo.
Results:
KHSRP expression was notably elevated in NSCLC cells. Overexpression of KHSRP remarkably promoted A549 cell proliferation, migration, and epithelial-mesenchymal transition (EMT); while KHSRP knockdown exhibited the opposite effects. Mechanically, KHSRP notably promoted the transcription of HMGB1 and upregulated its expression in A549 cells. Importantly, deficiency of KHSRP remarkably enhanced the suppressive effects of carboplatin on A549 cell proliferation, migration, EMT and HMGB1 expression. Meanwhile, in vivo experiments demonstrated that downregulation of KHSRP potentiated the inhibitory effect of carboplatin on tumor growth in tumor-bearing nude mice.
Conclusion:
These findings demonstrate that silencing of KHSRP enhances the drug sensitivity of carboplatin in NSCLC, potentially mediated through the inhibition of HMGB1. Targeting KHSRP may represent a promising therapeutic strategy to improve chemotherapy efficacy in NSCLC.
Insights
Silencing KHSRP enhances carboplatin sensitivity in non-small cell lung cancer (NSCLC) by inhibiting HMGB1. Targeting KHSRP offers a new strategy to improve chemotherapy efficacy for NSCLC patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Carboplatin resistance is a major challenge in non-small cell lung cancer (NSCLC) treatment.
- The role of KHSRP in NSCLC chemoresistance and its mechanism involving HMGB1 is not fully understood.
- KHSRP activates HMGB1 transcription, an oncogene affecting chemotherapy sensitivity.
Purpose of the Study:
- To investigate the role of KHSRP in NSCLC progression and carboplatin sensitivity.
- To determine if KHSRP affects NSCLC chemotherapy response through HMGB1.
- To explore KHSRP as a potential therapeutic target for NSCLC.
Main Methods:
- KHSRP expression analyzed by qRT-PCR in NSCLC cells.
- Cell proliferation, apoptosis, migration, and EMT assessed using various assays.
- Luciferase reporter assay to confirm KHSRP regulation of HMGB1.
- In vivo studies using A549 cell xenografts in nude mice.
Main Results:
- KHSRP expression is elevated in NSCLC cells and promotes proliferation, migration, and EMT.
- KHSRP overexpression upregulates HMGB1 transcription and expression.
- KHSRP deficiency enhances carboplatin's suppressive effects on NSCLC cells and tumor growth in vivo.
- Silencing KHSRP increases sensitivity to carboplatin in NSCLC.
Conclusions:
- KHSRP silencing enhances carboplatin drug sensitivity in NSCLC, likely via HMGB1 inhibition.
- Targeting KHSRP presents a promising therapeutic strategy to improve chemotherapy efficacy in NSCLC.
- Further research into KHSRP inhibition could lead to novel treatments for NSCLC.
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