FoxM1 expression was an independent poor prognostic factor in primary pulmonary squamous cell carcinoma

increased expression of foxm1 is correlated with non-small cell lung cancer

expression of Foxm1 in respiratory epithelial cells is critical for lung cancer formation and TOPO-2alpha expression in vivo, suggesting that Foxm1 is a promising target for anti-tumor therapy

The expression status of FOXM1 in non-small cell lung cancer is an independent prognostic factor and negatively correlated with prognosis.

FoxM1, p27(kip1) and p21(waf1/cip1) showed distinct immunoreactivity according to histological subtype, which may help in the differential diagnosis of pulmonary neuroendocrine tumours.

Suggest that FoxM1 plays an important role in the resistance of non-small-cell lung cancer cells to gefitinib in vitro.

We demonstrate that FoxM1 expression in NSCLC tumor tissues was associated with lung cancer recurrence.

Overexpression of FOXM1 is associated with lung carcinogenesis induced by low doses of arsenic.

We conclude that MnSOD may promote tumor aggressiveness via upregulation of the FoxM1-MMP2 axis, and that MnSOD expression can independently predict survival and relapse in patients with resected lung adenocarcinoma.

we suggest that FOXM1 may be a potential target for lung cancer therapy.

Findings indicate that FOXM1 may play an important role in advancing lung adenocarcinoma progression. Aberrant FOXM1 expression directly and constitutively activates SNAIL, thereby promoting lung adenocarcinoma metastasis.

regulated by the ERK pathway, mediates epithelial-mesenchymal transition in non-small cell lung cancer

Data show that siRNA knockdown of Forkhead box M1 (FOXM1) or microtubule-associated serine/threonine kinase-like (MASTL) induces radiosensitivity in non-small cell lung cancer (NSCLC).

this study shows that FOXM1 confers resistance to gefitinib in lung adenocarcinoma via a MET/AKT-dependent positive feedback loop

miR-361-5p acts as a tumor suppressor in lung cancer through down-regulation of FOXM1.

Study found that FOXM1 is a target of miR-149. miR-149 inhibited FOXM1 mRNA and protein expression levels by binding to its 3'-UTR in non-small cell lung cancer (NSCLC) cells. Moreover, patients with low expression levels of miR-149 exerted high FOXM1 mRNA levels.

Authors demonstrated that inhibition of either FOXM1 or AGR2 in human PIMAs inhibited mucinous characteristics, and reduced tumor growth and invasion. FOXM1 is necessary and sufficient to induce mucinous phenotypes in lung tumor cells in vivo.

FOXM1 knockdown reduced cell viability, migration, and invasion by propofol treatment plus miR-1284 suppression. In conclusion, our study indicated that propofol could inhibit cell viability, migration, invasion, and the EMT process in lung cancer cells by regulation of miR-1284.

In conclusion, our findings indicated that FOXM1 was highly expressed in lung cancer cells after exposure to ionizing radiation (IR). We also found that FOXM1 promoted radioresistance, invasion, migration, and EMT of lung cancer cells after IR, partly through upregulating KIF20A.

These findings revealed the role of forkhead box M1 upregulation by manganese superoxide dismutase overexpression in maintaining lung cancer stem-like cell properties. Therefore, inhibition of forkhead box M1 upregulation by manganese superoxide dismutase overexpression may represent an effective therapeutic strategy for non-small cell lung cancer.

The data indicate that MED28 interacts with FOXM1, and each affects the expression and localization of the other, and, more importantly, both regulate MMP2-dependent migration and invasion in human lung cancer cells.

Overexpression of FOXM1 might be associated with shorter overall survival of Chinese non-small cell lung cancer patients.[meta-analysis]

We demonstrate that low IGF2BP1 and FOXM1 expression can serve as a potential factor for the clinical diagnosis and prognosis of lung adenocarcinoma

Study found that all grades of lung adenocarcinoma (LUAD)tumors expressed higher levels of FOXM1. It as associated with worse prognosis. The overexpression of FOXM1 significantly promoted proliferation and its silencing inhibits the proliferation of LUAD cells. Also, FOXM1 was found to directly regulate the expression of CENPE in LUAD.

ALKBH5 affects the proliferation and invasion of lung adenocarcinoma cells under IH by downregulating m(6)A modification on FOXM1 mRNA and by promoting FOXM1 expression.

Long noncoding RNA HOXC-AS3 facilitates the progression of invasive mucinous adenocarcinomas of the lung via modulating FUS/FOXM1.

circFOXM1 promotes proliferation of non-small cell lung carcinoma cells by acting as a ceRNA to upregulate FAM83D.

Circ-MMP2 (circ-0039411) induced by FOXM1 promotes the proliferation and migration of lung adenocarcinoma cells in vitro and in vivo.

LncRNA NNT-AS1 promotes lung squamous cell carcinoma progression by regulating the miR-22/FOXM1 axis.

Transgenic expression of the forkhead box M1 transcription factor induces formation of lung tumors.

results suggest that endothelial-specific expression of FoxM1 limits lung inflammation and canonical Wnt signaling in lung epithelial cells, thereby restricting lung tumorigenesis

Data show that expression of Forkhead Box m1 (Foxm1) transcription factor in macrophages is required for pulmonary inflammation, recruitment of macrophages into tumor sites and lung tumor growth.

Data indicate that forkhead box M1 protein (FOXM1) is required for K-Ras-mediated lung tumorigenesis.