Abstract Aim To investigate the long non‐coding RNA DLG1 Antisense RNA 1 (lncRNA DLG1‐AS1) mechanism in cervical cancer cells with gemcitabine (GEM) resistance. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to detect DLG1‐AS1, miR‐16‐5p, and hepatoma‐derived growth factor (HDGF) expression in cervical cancer cells. The effects of DLG1‐AS1 knockdown on cell viability, proliferation, and apoptosis were investigated in GEM‐resistant cervical cancer cells. The binding of DLG1‐AS1 with miR‐16‐5p and of miR‐16‐5p with HDGF was confirmed through dual‐luciferase reporter assays. HDGF expression was detected through Western blotting. A xenograft model was established using stably transfected GEM‐resistant cervical cancer cells to detect the role of DLG1‐AS1 in tumorigenesis in vivo. Results DLG1‐AS1 expression was significantly elevated in HeLa/GEM and SiHa/GEM cells. DLG1‐AS1 silencing significantly reduced the viability and proliferation of GEM‐resistant cervical cancer cells. DLG1‐AS1 also promoted GEM sensitivity in cervical cancer cells by inhibiting miR‐16‐5p. Moreover, the tumor volume in nude mice in the DLG1‐AS1 knockdown group decreased after GEM treatment. In addition, DLG1‐AS1 targeted miR‐16‐5p, and miR‐16‐5p targeted HDGF. The miR‐16‐5p inhibitor reversed the DLG1‐AS1 knockdown effect in GEM‐resistant cervical cancer cells. Conclusion Knockdown of DLG1‐AS1 promoted GEM sensitivity in cervical cancer cells by regulating miR‐16‐5p/HDGF.
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