Overexpression of the LKB1 gene inhibits lung carcinoma cell proliferation partly through degradation of c-myc protein.

KRAS mutation-positive lung cancer displaying high levels of Myc could be treated by inhibiting Myc transactivation function.

miR-145 inhibits proliferation of non-small cell lung cancer cells through c-Myc

MYC amplification is a prognostic marker of patients with early-stage lung adenocarcinoma

Higher rates of the expressions of both APC and c-Myc proteins in non-small cell lung cancer primary foci were found compared with those in lymph node metastases.

Results thus identify a novel epigenetic mechanism by which MYC activates GATA4 leading to metastasis in lung adenocarcinoma.

MZF1-mediated MYC expression may promote tumor progression, resulting in poor outcomes in cases of lung adenocarcinoma with low-wild-type-LKB1 tumors.

c-MYC gain (but not chromosome 8 gain or c-MYC amplification) is an independent poor-prognostic factor for survival in lung adenocarcinomas.

the decrease in the expression of miR-29b by c-Myc may be responsible for FHIT loss-mediated tumor aggressiveness and for poor outcome in non-small cell lung cancer.

High c-myc expression was observed in non-small cell lung cancers.

MYC amplification is a frequent event in small cell lung cancer and is related to a short survival time.

USP37 is significantly upregulated in human lung cancer tissues, where its expression is positively correlated with c-Myc protein expression.

Results suggest that WT1 and c-MYC expression is important for survival in KRAS mutant tumors as opposed to KRAS wild-type non-small cell lung tumors.

Our results confirm MYC as frequently amplified in early-stage non-small cell lung cancer

a link between MYC and mTOR-independent eIF4E contribute to the resistance to everolimus in SCLC cells. Control of the MYC-eIF4E axis may be a novel therapeutic strategy for everolimus action in small cell lung cancer

Increased c-myc is associated with invasiveness in Non-small Cell lung cancer.

protein pairs significantly correlated with an increased risk of death in non-small cell lung cancer: c-Myc with p16, c-Myc with mSin3A

Mechanistic studies indicated that PAF1C could promote lung cancer cell proliferation through regulating c-MYC transcription.

MYC gene family of transcription factors may be a targetable entity to test new therapies against, in particular, aurora kinase inhibitors.Epigentic processes, such as gene promoter methylation and histone acetylation, may be candidate targets to test in small cell lung cancer (SCLC)

non-small cell lung cancer savolitinib resistance arises via multiple mechanisms that converge on MET-independent mTOR and MYC activation

High MYC expression is associated with lung cancer.

Role of c-myc signaling in in lung adenocarcinoma cells.

High Myc expression is associated with lung cancer.

Results indicate that spliceosome inhibitors would be promising molecular target drugs in small cell lung cancer (SCLC) irrespective of the myc proto-oncogene protein (MYC) status.

Combined, these findings suggest that c-Myc could transcriptionally regulate TCRP1 in cell lines and clinical samples and identified the c-Myc-TCRP1 axis as a negative biomarker of prognosis in tongue and lung cancers.

High myc expression is associated with lung cancer.

a phosphorylation mutant form of Mxi1 (Mxi1-S160A), which cannot be degraded by S6K1 and beta-Trcp, is much more stable and efficient in suppressing the transcriptional activity of Myc and radioresistance in lung cancer cells.

Circular RNA hsa_circRNA_103809 promotes lung cancer progression via facilitating ZNF121-dependent MYC expression by sequestering miR-4302.

TP53 mutations define a subset of ALK-translocated non-small cell lung carcinoma tumours with recurrent MYC amplication that harbour chromosomal instability, leading to the co-occurrence of pathogenic aberrations.

expression and Clinical Significance of LC-3 and P62 in Non-small Cell lung cancer

Oncogenic zinc finger protein ZNF322A promotes stem cell-like properties in lung cancer through transcriptional suppression of c-Myc expression.

we revealed that CPA4 downregulation may induce apoptosis and G1-S arrest by suppressing the protein kinase B/c-MYC pathway. These results suggest that CPA4 has an oncogenic effect on lung cancer growth. Taken together, we identified a novel gene in lung cancer that might provide a basis for new therapeutic targets.

C-myc/miR-150/EPG5 axis mediated dysfunction of autophagy promotes development of non-small cell lung cancer.

High C-MYC expression is associated with non-small cell lung cancer.

c-Myc shuttled by tumour-derived extracellular vesicles promotes lung bronchial cell proliferation through miR-19b and miR-92a.

MiR-1827 functions as a tumor suppressor in lung adenocarcinoma by targeting MYC and FAM83F.

Multi-Omics Analysis Identifies MGA as a Negative Regulator of the MYC pathway in lung Adenocarcinoma.

STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/betacatenin pathway and feedback regulation by cmyc.

CPF impedes cell cycle re-entry of quiescent lung cancer cells through transcriptional suppression of FACT and c-MYC.

MYC Drives Temporal Evolution of Small Cell lung cancer Subtypes by Reprogramming Neuroendocrine Fate.

Biomarker-driven phase 2 umbrella trial study for patients with recurrent small cell lung cancer failing platinum-based chemotherapy.

A novel TRPM7/O-GlcNAc axis mediates tumour cell motility and metastasis by stabilising c-Myc and caveolin-1 in lung carcinoma.

Myc inhibition triggers rapid regression of incipient and established lung tumours, defining an unexpected role for endogenous Myc function in the maintenance of Ras-dependent tumours in vivo

MYC is a metastasis gene for non-small-cell lung cancer

MYC inactivation restores BRAF(V600E)-induced senescence in lung tumors in mice.

Report gene regulatory networks controlling expression of cell cycle and apoptosis regulated genes in a transgenic mouse model of papillary lung adenocarcinomas.

our results show how MYC drives the production of specific eicosanoids critical for lung cancer cell survival and proliferation

In a mouse lung model of KRas(G12D)-driven adenomas, co-activation of Myc drives the immediate transition to highly proliferative and invasive adenocarcinomas marked by highly inflammatory, angiogenic, and immune-suppressed stroma.