Objective The aim of this study is to systematically evaluate the expression level of lncRNA MIR205HG in non-small cell lung cancer (NSCLC) patients and its association with clinical features, and further explore whether MIR205HG affects the resistance of lung cancer cells to gemcitabine by regulating KLF5, thereby providing potential molecular targets for overcoming chemotherapy resistance. Methods Data from 81 NSCLC patients admitted to our thoracic surgery department from October 2019 to May 2021 were reviewed. The expression levels were compared in tumor tissue and adjacent tissues, and the prognosis of patients with different levels of expression of expression of expression of MIR205HG was compared. Survival analysis was also conducted. In vitro detection of MIR205HG expression levels in lung cancer cell lines, construction of MIR205HG overexpression and knockdown lung cancer cells, CCK-8 detection of cell proliferation, clone formation assay to detect cell clone formation ability, qRT PCR and Western blot detection of MIR205HG and KLF5 mRNA and protein expression. Compare the sensitivity of in in gemcitabine drug in SK-MES-1 and gemcitabine resistant cells (SK-MES-1/GR) and detect MIR205HG and KLF5 mRNA and protein expression levels in SK-MES-1 and SK-MES-1/GR. Using SK-MES-1/GR cells transfected with MIR205HG interference plasmid to detect gemcitabine drug sensitivity and KLF5 mRNA and protein expression levels. Results The expression level of MIR205HG in tumor tissue was higher than that of adjacent tissues. High expression of MIR205HG is associated with increased tumor staging and lymph node metastasis in patients. The prognosis of the MIR205HG high expression group was worse. The expression of MIR205HG in lung cancer cell lines SK-MES-1, NCI-H1703, NCI-H2170 and NCI-H226 was higher than in BEAS-2B cells. Inhibition of MIR205HG suppresses cell proliferation and colony formation ability of cells, and down-regulates the expression level of KLF5. The expression levels of MIR205HG and KLF5 were up-regulated in SK-MES-1/GR, and inhibition of MIR205HG increased cell sensitivity to gemcitabine. Conclusion MIR205HG is highly expressed in NSCLC and is associated with poor prognosis, suggesting its potential as a prognostic biomarker for adverse outcomes in NSCLC. The MIR205HG/KLF5 signaling axis serves as a key pathway mediating gemcitabine resistance in NSCLC. Targeting this axis holds promise as a novel strategy to overcome gemcitabine resistance in NSCLC.
Key words
MIR205HG /
KLF5 /
non-small cell lung cancer /
gemcitabine /
drug resistance
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