Inactivation of LKB1/STK11 is a common event in adenocarcinomas of the lung.

This reports for the first time the presence of frequent LKB1 inactivating mutations in human lung cancer.

loss of function mutations in LKB1 may also be frequently involved in the pathogenesis of large cell lung carcinomas

PEA3 stabilization due to LKB1 inactivation could lead to epithelial/mesenchymal transition and greater lung cancer invasion potential.

somatic LKB1 genetic alterations preferentially occur in a subset of poorly differentiated lung adenocarcinomas that appear to correlate with smoking males

inactivation of LKB1 was found in 34% and 19% of 144 analysed human lung adenocarcinomas and squamous cell carcinomas, respectively

LKB1 gene mutations were relatively rare in Japanese patients with lung cancer compared with Caucasian patients.

Down-regulation of LKB1 gene expression can stimulate malignant biological behavior of lung carcinoma cells.

Marked reduction of LKB1 expression in high-grade neuroendocrine tumors of the lung suggests a possible role of LKB1 inactivation in its tumorigenesis.

LKB1 interacts only with active form of cdc42 and PAK, but not with inactive cdc42. Taken together, these results show that LKB1 is a critical mediator of the NSCLC polarity program in lung cancer cells through a novel LKB1-cdc42-PAK pathway.

LKB1 may have a role in lung cancer [review]

LKB1 and KRAS mutation is associated with lung cancers and show sensitivity to the mTOR and MEK inhibitors.

LKB1 has now been demonstrated to play a crucial role in pulmonary tumorigenesis, controlling initiation, differentiation, and metastasis. Review.

Somatic alterations of the serine/threonine kinase LKB1 gene in squamous cell and large cell lung carcinoma.

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

LKB1 serine-threonine kinase is a tumor suppressor that is inactivated in a large number of sporadic human lung non-small cell carcinomas and cervical cancers.

involved of in epithelial-mesenchymal transition of lung cancer cells

LKB1 mutations are associated with lung adenocarcinomas.

LKB1 loss of function promotes lung cancer malignancy through remodeling of extracellular matrix microenvironment, and identify LOX as a potential target for disease treatment in lung cancer patients.

review summarizes LKB1-dependent invasion pathways where compromised LKB1 function could promote non-small cell lung cancer metastasis(REVIEW)

The LKB1 gene alteration is rare in Japanese patients with lung adenocarcinoma, and is generally limited to male smokers.

The relatively high frequency of LKB1 mutations in mucinous bronchioloalveolar carcinoma patients may therefore suggest its involvement in lung carcinogenesis, at least in mucinous bronchioloalveolar carcinoma.

The lower rate of LKB1 somatic mutations in lung adenocarcinomas are characteristic of the Kujukuri cohort as compared to Caucasians.

targets in LKB1 signaling pathway for non-small cell lung cancer therapy

Data suggest that macrophage migration inhibitory factor (MIF) and d-dopachrome tautomerase (d-DT) act cooperatively to inhibit steady-state phosphorylation and activation of AMPK in LKB1 wild type and LKB1 mutant non-small cell lung carcinomas cells.

CRTC1-NEDD9 signaling axis mediates lung cancer progression caused by LKB1 loss.

mutation of LKB1 is associated with lung adenocarcinoma.

mutations may confer resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in lung adenocarcinoma patients

Study concludes that suppression of lung cancer cell invasion by LKB1 through downregulation of TF and VEGF may partly depend on its inhibitory effect on the transcription factor Sp1.

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

Loss of LKB1 defines a subset of lung adenocarcinomas associated with characteristic molecular phenotypes and distinctive gene expression features.

Endoplasmic reticulum stress activators represent a potential treatment avenue for non-small cell lung cancers deficient in LKB1.

The knockdown of PDE4D gene expression inhibited proliferation of STK11-mutated lung cancer lines. Furthermore, challenge with a panel of PDE4-specific inhibitors was shown to selectively reduce the growth of STK11-mutated lung cancer lines.

Study demonstrated that expression of LKB1 and Beclin1 was reduced in non-small cell lung cancer (NSCLC) tissues, and the reduced expression of these proteins, is an independent indicator for the overall survival of NSCLC patients.

STK11 mutations were associated with stage IV lung adenocarcinoma adrenal metastases.

Disruption of BASIGIN decreases lactic acid export and sensitizes non-small cell lung cancer to biguanides independently of the LKB1 status.

LKB1 gene inactivation in non-small cell lung cancer cells does not increase the sensitivity to the mTOR inhibitors.

All together our results show that STK11ex1-2 mutations delineate an aggressive subtype of lung cancer for which a targeted treatment through STK11 inhibition might offer new opportunities.

Decreased LKB1 expression is associated with metastatic endometrial and lung cancers.

STK11 mutation is associated with lung Adenocarcinoma.

identified focally upregulated FAK and collagen-associated collective invasion in KRAS and LKB1 comutated human lung adenocarcinoma patients. Our results suggest that patients with LKB1 mutant tumors should be stratified for early treatment with FAK inhibitors

CPS1 maintains pyrimidine pools and DNA synthesis in KRAS/LKB1-mutant lung cancer cells

Low LKB1 expression is associated with non-small cell lung cancer.

Our results indicate that HPV16 E6/E7 indirectly upregulated the expression of VEGF by inhibition of liver kinase B1 expression and upregulation of hypoxia-inducible factor 2alpha expression,thus propose a human papillomavirus-liver kinase B1-hypoxia-inducible factor 2A-vascular endothelial growth factor axis for the tumorigenesis of lung cancer

E6 upregulation of hTERT by downregulated LKB1 and upregulated SP1 in lung cancer cells. These results indicated that E6 played a predominant role in the regulation of telomerase activation and may be a valuable therapeutic targets for HPV-related cancer.

LKB1 undergoes AURKA-mediated phosphorylation, which largely compromises the LKB1/AMPK signaling axis, in turn leading to the elevation of non-small cell lung cancer cell proliferation, invasion and migration.

LKB1 performed as a tumor suppressor in lung cancer inhibiting proliferation of lung cancer cells and inducing their apoptosis. LKB1 also inhibited the in vivo growth of lung cancer. After treatment with cyclopamine, the activated Shh signaling pathway induced by LKB1 silencing was suppressed, and the inactivated Shh signaling pathway induced by LKB1 over-expression was enhanced.

STK11/LKB1 mutations are found to be the most prevalent genomic driver of primary resistance to PD-1 axis inhibitors in KRAS-mutant lung adenocarcinoma.

Cytoplasmic LKB1 promotes the growth of lung adenocarcinoma and could be a prognostic marker for lung adenocarcinoma.

There were significantly expressed differences in the ubiquitin-related gene SH3RF1 between the LKB1 mutant and wild-type lung adenocarcinoma patients (p = 9.78013E-05). Patients with LKB1 mutation and high expression of SH3RF1 had a better prognosis than the low expression group (HR 0.356, 95% CI 0.136-0.929, p = 0.035). SH3RF1 can influence cell cycle, apoptosis, DNA replication and the p53 signaling pathway.

LKB1 deficiency induces an autocrine INSL4 signaling that critically supports the growth and survival of lung cancer cells. Therefore, aberrant INSL4 signaling is a promising therapeutic target for LKB1-deficient lung cancers.

LKB1 inhibits the metastasis and angiogenesis of lung cancer through suppressing the Shh signaling pathway

Study reports that JNK1/2 activities attenuate LKB1-deficiency-driven lung squamous cell carcinoma (LSCC) initiation and progression through repressing DeltaNp63 signaling. LSCC patients with higher JNK1/2 activities have better survival rates and activating JNK1/2 activities attenuate LSCC progression.

An LKB1-SIK Axis Suppresses lung tumor Growth and Controls Differentiation.

CRTC2 is unphosphorylated and therefore constitutively activated in LKB1-mutant non-small cell lung cance, where it promotes tumor growth, in part via the induction of the inhibitor of DNA binding 1.

Mir-451 inhibits proliferation and migration of non-small cell lung cancer cells via targeting LKB1/AMPK.

The prevalence and prognostic value of KRAS co-mutation subtypes in Chinese advanced non-small cell lung cancer patients.

Less immune cell infiltration and worse prognosis after immunotherapy for patients with lung adenocarcinoma who harbored STK11 mutation.

The hexosamine biosynthesis pathway is a targetable liability in KRAS/LKB1 mutant lung cancer.

Lkb1 is a potent suppressor of carcinogen-induced skin and lung cancers and downstream targets beyond the AMPK-mTOR pathway are likely mediators of Lkb1-dependent tumor suppression.

Genetic deletion of LKB1 in various mouse tissues results in tumorigenesis, and loss of LKB1 increases metastasis in a mouse model of lung non-small cell carcinoma.

Loss of LKB1 is associated with therapeutic response of non-small cell lung cancer.

LKB1 haploinsufficiency as a risk factor for tumor progression of BRAF(V600E) mutated lung adenomas in human cancer patients

Lkb1-deficient lung adenocarcinoma progressively transdifferentiates into squamous cell carcinoma.

biallelic inactivation of Lkb1 and Pten in the mouse lung leads to lung squamous cell carcinoma that recapitulates the histology, gene expression, and microenvironment found in human disease.

Data show that that the lineage switching of KRAS+ lung adenocarcinomas (ADC) to squamous cell carcinoma (SCC) through deletion of liver kinase B1 Lkb1 (Stk11).