DDX11-AS1 Modulates Dna Damage Repair to Enhance Paclitaxel Resistance of Lung Adenocarcinoma Cells

Abstract

Aim: To investigate the influence of DDX11-AS1 on paclitaxel (PTX) resistance in lung adenocarcinoma (LUAD). Methods: LncRNA expression and functional enrichment analyses were processed via bioinformatics methods. DDX11-AS1 expression was detected via quantitative real-time PCR. Cell counting kit-8, colony formation, flow cytometry and comet assays were manipulated to measure cell proliferation, apoptosis, cell cycle and DNA damage repair, respectively. Western blot was used to assess DNA damage-related protein expression. Results:DDX11-AS1 was in a high expression status in LUAD, and could promote LUAD cell proliferation and PTX resistance, while suppressing cell apoptosis. DNA damage repairing ability was also modulated by the change of DDX11-AS1 expression. Conclusion: LncRNA DDX11-AS1 promotes DNA damage repair to enhance PTX resistance in LUAD.

Keywords::

• DDX11-AS1
• DNA damage repair
• lung adenocarcinoma
• paclitaxel
• resistance

Author contributions

J Liu conceived and designed the study. X Yang, S Gao and M Wen performed the experiments. Q Yu wrote the paper. J Liu, X Yang, S Gao and M Wen reviewed and edited the manuscript. All authors read and approved the manuscript.

Financial & competing interests disclosure

This study was supported in part by grants from the Public Welfare Fund of Jinhua Science and Technology Bureau of Zhejiang Province (grant no. 2020-4-076). The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Consent for publication

All authors consent to submit the manuscript for publication.

Availability of date & materials

The date and materials in the current study are available from the corresponding author on reasonable request.

Additional information

Funding

This study was supported in part by grants from the Public Welfare Fund of Jinhua Science and Technology Bureau of Zhejiang Province (grant no. 2020-4-076). The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.