Patients with previously treated advanced KRAS mutant NSCLC were prospectively assigned to one of four molecularly defined cohorts based on the presence or absence of TP53 or CDKN2A alterations and received treatment with defactinib 400 mg orally BID until disease progression or intolerable toxicity.
<b>Purpose:</b> To evaluate the effect of NU7026, a specific inhibitor of DNA-PKcs, on DNA-double strand break (DSB) repair in a cell cycle specific manner, on the G2/M checkpoint, mitotic progression, apoptosis and clonogenic survival in non-small-cell lung carcinoma (NSCLC) cell lines with different p53 status.
Knockdown of p53 attenuated the ability of SNF to inhibit anoikis resistance and sphere formation in A549 cancer cells, suggesting that the presence of p53 in NSCLC cancer cells is involved in the sensitivity to SFN.
In multiple NSCLC cell lines with varied p53 and EGFR status, we compared and examined the protein contents involved in EGFR-Akt-P53 signaling loop (EGFR, P-EGFR, Akt, P-Akt, p53, P-p53) by Western blot.
Mechanistically, p53 restricts L1CAM expression through the β-catenin/Slug pathway, with levels of β-catenin and Slug positively correlating with L1CAM expression in NSCLC tumors.
Upregulation of miR-675-5p induced by lncRNA H19 was associated with tumor progression and development by targeting tumor suppressor p53 in non-small cell lung cancer.
In this study, the involvement of p53 in the cell cycle arrest and pro-apoptotic action of actinomycin V was investigated in human non-small-cell lung carcinoma A549 cells.
Taken together, our results demonstrate SMYD2 is involved into cisplatin resistance through regulating p53 pathway, and might become a promising therapeutic target for cisplatin resistance in NSCLC.
<b>Methods:</b> Three NSCLC cell lines, H1299 (deleted p53), A549 (wild-type p53), and H23 (mutated p53), were examined in the present investigation to represent NSCLC with different p53 functions.
The expression of p53 in the tumor tissue of NSCLC patients was significantly reduced in comparison with PTLC, and its expression was negatively correlated with the pathological stage, lymph node metastasis, and was positively correlated with the degree of differentiation.