Mcl-1 protein is overexpressed in a subset of human NSCLC and enhanced levels of Mcl-1 may protect lung cancer cells from death induced by a variety of pro-apoptotic stimuli.

HPV 16/18 up-regulates the expression of interleukin-6 and antiapoptotic Mcl-1 in non-small cell lung cancer

common variants in MCL1 promoter correlated with increased transactivation in solid cancer cells and were associated with reduced risk of lung cancer in nonsmokers.

MiR-101 and Mcl-1 may play important roles as biomarkers for prognosis and therapeutic targets in non-small cell lung cancer

betaArr1 and Mcl-1 are involved in the self-renewal and expansion of non-small cell lung carcinoma -cancer stem cells and are potential targets for anti-cancer therapy.

Studied the possible role of miRNAs in the development of drug resistance in human lung cancer cell line and found that miR-135a/b were downregulated while MCL1 was upregulated in A549/CDDP (cisplatin) cells, compared with the parental A549 cells.

Noxa recruits MCL-1 from the cytosol to the mitochondria modulating ABT-737 sensitivity in small cell lung cancer.

These data suggest that an interaction between Mcl-1 and VDAC promotes lung cancer cell migration by a mechanism that involves Ca(2+)-dependent reactive oxygen species production.

Results identified MCL-1 as a key molecule for acquiring epithelial-to-mesenchymal transition-associated chemo-resistance in human non-small cell lung cancer.

These data support the use of MCL1 expression as a predictive biomarker for USP9X inhibitors in non-small cell lung cancer therapy

MiR-205/miR-218 expression is associated with carboplatin chemoresistance and regulation of apoptosis via Mcl-1 and survivin signaling in lung cancer cells.

mTOR complex 2 regulates cell survival and growth in non-small-cell lung cancer (NSCLC) cell lines by stabilizing Mcl1.

Results indicated that the pro-survival Bcl-2 family protein MCL-1 may be the key target for reversing the cisplatin-resistance in non-small cell lung cancer cells.

these findings provided that in lung cancer cells, tumor suppressor miR-451 enhanced DPP sensitivity via regulation of Mcl-1 expression, which could be served as a novel therapeutic target for the treatment of chemotherapy resistant in lung cancer.

MCL1 has a role in lung cancer cell survival via chaperone-mediated autophagy

Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant non-small cell lung cancer (NSCLC)cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291

Deubiquitinating enzyme 13 (USP13) regulates myeloid cell leukemia sequence 1 protein (MCL1) stability in lung and ovarian cancer cells.

cMcl-1 overexpression appears to occur independently from MCL1 gene amplification in nonsmall cell lung cancer and correlates with adenocarcinoma in situ histologic type, lower tumor grade, smaller tumor size, nonrecurrent disease, and increased survival.

This work has defined EGFR mutations and AKT phosphorylation as markers for sensitivity to combined MCL-1 and BCL-2/xL targeted therapy and establishes a rationale to explore multiple BCL-2 family members in patients who are refractory to EGFR inhibitor treatment. Our data support the design of a clinical trial that aims to employ inhibitors of the BCL-2 family of proteins in lung cancer patients.

Elevated expression of Mcl-1 might be inversely proportional to disease progression of non-small cell lung cancer patients by promoting cell proliferation and inhibiting apoptosis

Study discovered a cross-talk between Mcl-1 and Akt in promoting lung cancer cell growth. Depletion of endogenous Mcl-1 from human lung cancer cells using CRISPR/Cas9 or Mcl-1 shRNA significantly decreased Akt activity, leading to suppression of lung cancer cell growth in vitro and in xenografts. Mechanistically, Mcl-1 directly interacted via its PEST domain with Akt at the pleckstrin homology (PH) domain.

EGFR-independent EGFR-mutant lung adenocarcinoma cells depend on Bcl-xL and MCL1 for survival.

MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically.

NCAPH is negatively associated with Mcl1 in nonsmall cell lung cancer.