SOX2 regulates paclitaxel resistance of A549 non‑small cell lung cancer cells via promoting transcription of ClC‑3

miR-199a-5p targets DUSP14 to regulate cell proliferation, invasion and stemness in non-small cell lung cancer

“…Stemness is closely related to acquired resistance. The upregulation of stemness-related proteins SOX2 and OCT4 modulates resistance to chemotherapeutic drugs, such as paclitaxel and gefitinib [ 30 , 31 ]. Our data suggest that high expression of DUSP14 is required to sustain the aggressiveness and stemness in NSCLC cells, since the knockdown of DUSP14 reduced cell growth, invasion, sphere-forming ability, as well as the protein levels of stem cell markers (SOX2 and OCT4).…”

CXCR2 inhibition overcomes ponatinib intolerance by eradicating chronic myeloid leukemic stem cells through PI3K/Akt/mTOR and dipeptidylpeptidase Ⅳ (CD26)

“…Both SOX2 and c-Myc are transcription factors that, when overexpressed in tumor cells, promote tumor growth, metastasis, chemoresistance, and stemness, thereby contributing to the acquisition of CSC properties [ 48 , 49 ]. Importantly, SOX2-expressing cancer cells often exhibit elevated levels of CSC markers and are associated with poor prognoses [ [50] , [51] , [52] , [53] , [54] ]. Similarly, c-Myc overexpression is observed in various cancers, driving cancer stem cell-like traits and aggressive disease progression [ 55 , 56 ].…”

circPDK1 competitively binds miR-4731-5p to mediate GIGYF1 expression and increase paclitaxel sensitivity in non-small cell lung cancer

“…PTX-resistant A549/PTX cell line was established by exposing A549 cells to increasing concentrations of PTX (50 nM-250 nM). To maintain the PTX-resistant phenotype of A549/PTX cells, 0.1 μM PTX was added to the culture medium and routinely cultured overnight (5% CO 2 , 37 °C) [ 31 ].…”