Stat3 has a role in transducing survival signals downstream of tyrosine kinases such as Src, EGF-R, and c-Met, as well as cytokines such as IL-6, in human nonsmall cell lung cancers

Cyclooxygenase-2-dependent activation of STAT3 by interleukin-6 has a role in non-small cell lung cancer

These results suggest a relevant role for STAT5 and Bcl-xL as apoptosis-regulatory proteins in the pathogenesis of lung cancer, and overexpression of both Neu and activated STAT3, could be related with the proliferation rate in lung carcinoma cells.

EGFR could activate the gp130/JAK/STAT3 pathway by means of IL-6 upregulation in primary human lung adenocarcinomas, making this pathway a potential target for cancer treatment.

Stat3 is a potent oncogenic molecule that plays a role in formation of lung adenocarcinomas in both mice and humans.

constitutively activated STAT3 regulates expression of MUC1, which mediates lung cancer cell survival and metastasis in vitro and in vivo.

analysis of reciprocal regulation of c-Src and STAT3 in non-small cell lung cancer

Abundant tyrosine phosphorylation of STAT3 leads to primary resistance to EGFR inhibitors in lung cancer.

Loss of STAT3 activity in lung cancer cells resulted in reduced cell proliferation and apoptosis and combined EGFR and STAT3 loss had additional antitumor effects.

mediates tumor angiogenesis by upregulation of VEGF and bFGF in non-small-cell lung cancer

Data show that ALK inhibitor-induced apoptosis is mediated both by BIM upregulation resulting from inhibition of ERK signaling as well as by survivin downregulation resulting from inhibition of STAT3 signaling in EML4-ALK-positive lung cancer cells.

The JAK2/STAT3 signaling pathway plays an important role in the angiogenesis of non-small cell lung cancer.

Activation of the signal transducer and activator of transcription 3 pathway up-regulates estrogen receptor-beta expression in lung adenocarcinoma cells

CK2 inhibitors enhance the radiosensitivity of human non-small cell lung cancer cells through inhibition of stat3 activation

polymorphisms in the STAT3 gene may have a protective role in the development of non-small cell lung cancer (NSCLC), particular of stage III/IV NSCLC

Our results suggest that p-STAT3 is an important factor during carcinogenesis and metastasis of lung carcinoma.

JAK2/STAT3 signaling operates independent of known driver mutations in non-small cell lung carcinoma and plays critical roles in tumor cell behavior that may not be effectively inhibited by drugs that selectively target these driver mutations.

the expression of phosphorylated STAT3 (pSTAT3) in non-small cell lung cancer

Results show that accumulation of pSTAT3-Tyr705 promotes EGFR L858R mutant cell death, thereby confirming the existence of a STAT3-dependent pro-apoptotic pathway in these lung cancer cells.

endogenous STAT3 expression is a determinant of intrinsic taxane resistance in lung cancer.

The expression levels of STAT3, P-STAT3, and VEGF-C were higher in small cell lung cancer than in normal tissue; STAT3 and VEGF-C play important roles in the development of small cell lung cancers

STAT3 is not crucial for the control of basal cell proliferation and survival of lung carcinoma cells but modulates susceptibility to DNA damaging chemotherapeutics by regulation of intrinsic pro-survival pathways.

Stat3 downstream gene product chitinase 3-like 1 is elevated in lung cancer

AGK expression was significantly correlated with JAK2/STAT3 hyperactivation in esophageal squamous cell carcinoma, as well as in lung and breast cancer.

These findings uncover a novel mechanism of erlotinib resistance and provide a novel approach to overcome resistance by blocking the STAT3/Bcl2/Bcl-XL survival signaling pathway in human lung cancer

Confluence of cultured lung cancer cells dramatically increases STAT3 activation independent of SRC action.

Review of the contribution of STAT3 to lung cancer growth and progression. [Review]

Thus, our results suggest a previously unknown Stat3-PTPN13 molecular network controlling squamous cell lung carcinoma development

STAT3 protein expression is a strong indicator of poor prognosis and survival of patients diagnosed with non-small-cell lung cancer. phospho-STAT3(review)

It has been shown that rs3816769 STAT3 gene polymorphisms are associated with Nonsmall cell lung cancer susceptibility and might be regarded as having a significant functional and diagnostic value.

in this work, we identified TPCA-1 as a direct dual inhibitor for both IKKs and STAT3, whereas treatment targeting EGFR only could not sufficiently repress NF-kappaB and STAT3 pathways for lung cancers harboring mutant EGFR

Blockage of Stat3 with a selective inhibitor, S3I-201, or siRNA presents an effective strategy to overcome resistance to PI3K/Akt/mTOR inhibition in non small-cell lung cancer cells.

Studied a new therapeutic alternative in the treatment of multiresistant lung adenocarcinoma via siRNA-specific transfection of six crucial molecules involved in lung carcinogenesis: SFR, E2F1, Survivin, HIF1, HIF2 and STAT3.

High STAT3 expression is associated with non-small-cell lung cancer.

our results suggest that the activated Stat3 may represent an important mechanism for Beclin 1 downregulation in nonsmall cell lung cancer development

the E3 ubiquitin ligase seven-in-absentia-2 (SIAH2) accelerates the proteasomal degradation of TYK which consequently suppresses the activation of STAT3 in non-small-cell lung cancer

High Stat3 protein expression is associated with lung cancer.

Cten expression mediates invasion of human lung cancer cells and is upregulated by epidermal growth factor via STAT3.

Increased expression of the Th17-IL-6R/pSTAT3/BATF/RorgammaT-axis in the tumoural region of adenocarcinoma as compared to squamous cell carcinoma of the lung

signalings can reciprocally and positively regulate each other, leading to enhanced non-small cell lung cancer (NSCLC) cell proliferation and survival.

our findings suggest that miR-124 functions as a tumor suppressor by targeting STAT3, and that miR-124 may potentially serve as a useful biomarker for the prognosis of non-small cell lung cancer patients.

MicroRNA-10a silencing reverses cisplatin resistance in the A549/cisplatin human lung cancer cell line via the transforming growth factor-beta/Smad2/STAT3/STAT5 pathway

MicroRNA-19a functions as an oncogenic microRNA in non-small cell lung cancer by targeting the suppressor of cytokine signaling 1 and mediating STAT3 activation

STAT3 and miR-21 are cooperative regulators of stemness, migration and tumor initiation in lung-derived brain metastasis

Data show that crizotinib can induce cytoprotective autophagy by suppression of STAT3 transcription factor in lung cancer cells.

Antisense oligonucleotide AZD9150 decreased STAT3 expression in a broad range of preclinical cancer models and showed antitumor activity in lymphoma and lung cancer models.

Using Fgfr4 single nucleotide polymorphism knock-in mice and transgenic mouse models for breast and lung cancers, we validate the enhanced STAT3 signalling induced by the FGFR4 Arg388-variant in vivo

Data indicate that EPHA3 is involved in regulating the multidrug resistance (MDR) of small cell lung cancer (SCLC) via PI3K/BMX/STAT3 signaling and may be a therapeutic target in SCLC.

Cyclosporine A dramatically increased gefitinib-induced apoptosis in primary sensitive, primary resistant and acquired resistance non-small cell lung cancer cells viat STAT3 inhibition.

Data show that astaxanthin functions as a potent inhibitor of A549 lung cancer cell growth by targeting Janus kinase 1 a(JAK1)/STAT3 transcription factor (STAT3) signaling pathway.

Findings indicate the importance of Src-Stat3 signaling cascade in gallic acid (GA)-mediated tumor-suppression activity and a therapeutic insight of GA for acquired resistance to EGF receptor tyrosine kinase inhibitors in lung cancer.

High STAT3 expression is associated with lung cancer.

MAPK signaling may control the expression of PD-L1 and several genes related to enhanced cell motility. Our findings suggest that MAPK, along with STAT3, is important for determining PD-L1 expression, which could be useful for targeted therapies against lung cancers.

cancer-associated fibroblasts treated with cisplatin facilitate chemoresistance of lung adenocarcinoma through IL-11/IL-11R/STAT3 signaling pathway.

Study uncovers a coordinated signaling network centered on both STAT3 and Src-YAP signaling that limits targeted therapy response in lung cancer and identifies an unforeseen rational upfront polytherapy strategy to minimize residual disease and enhance clinical outcomes.

that loss of RIP4 enhances STAT3 signaling in lung cancer cells

Taken together, mir-125a-5p inhibited the proliferation and invasion of lung cancer cells and facilitated lung cancer cell apoptosis through suppressing STAT3. Enhancing the expression of miR-125a-5p is expected to benefit the therapy for the patients with lung cancer.

p-STAT3 overexpression has significant correlation with poorer overall survival of lung cancer patients, as well as with more advanced TNM stages and lymph node metastasis. [meta-analysis]

Studied the tumor suppressive role and antiproliferative effect of MicroRNA-218 in lung cancer cells through targeting of IL-6/STAT3 pathway.

PAI-1 was identified as the target gene of miR-34a and activated the Stat3 signaling pathway to promote epithelial-mesenchymal transition in non-small cell lung cancer cells.

STAT3 expression is regulated by miR-26a in ambient particulate matter-bound metal-triggered lung cancer.

Mir-204 attenuates angiogenesis in lung adenocarcinoma via JAK2-STAT3 pathway.

MicroRNA-454 inhibits non-small cell lung cancer cells growth and metastasis via targeting expression of STAT3.

we revisited the question of the relationship between Cav1 and Stat3-ptyr705 in non-transformed mouse fibroblasts and in human lung carcinoma cells, by examining their effect at different cell densities.Our results demonstrate that Cav1 downregulates cadherin-11, by a mechanism which requires the Cav1 scaffolding domain. This cadherin-11 downregulation, leads to a reduction in cRac1 and Stat3 activity levels.

we wanted to explore whether STAT3 can be related to lymph node micrometastasis of non-small cell lung cancer (NSCLC). To address this question, we evaluated the expression of MUC1 mRNA in the lymph node samples of NSCLC to determine micrometastasis. Then, we evaluated what role STAT3 overexpression plays in lymph node micrometastasis of NSCLC.

Our results showed that IL-37 plays an inhibitory role in non-small cell lung cancer progression, possibly by suppressing STAT3 activation and decreasing epithelial-to-mesenchymal transition by inhibiting IL-6 expression. IL-37 could serve as a potential novel tumor suppressor in non-small cell lung cancer

H19 may serve as a competing endogenous RNA (ceRNA) to modulate STAT3 by attaching miR-17 in lung cancer

High STAT3 expression is associated with lung adenocarcinoma.

High STAT3 expression is associated with lung adenocarcinoma.

These data underscore a critical sex-specific role for epithelial Stat3 signaling in K-ras mutant lung adenocarcinomas.

PLOD3 and the STAT3 pathway were significantly correlated in the metastatic foci of lung cancer patients; PLOD3-STAT3 levels were highly correlated with a poor prognosis. These results indicate that PLOD3 promotes lung cancer metastasis in a RAS-MAP kinase pathway-independent manner.

Scutellarin (SCU) can suppress proliferation and promote apoptosis in A549 cells through AKT/mTOR/4EBP1 and STAT3 pathways. This suggests that SCU may be developed into a promising antitumor agent for treating non-small cell lung cancer (NSCLC)

The association between STAT3 single nucleotide polymorphism rs4796793 and susceptibility to lung cancer in Chinese lung cancer patients.

the results of the present study indicated that lncRNA H19/miR29b3p/STAT3 signaling was involved in the development of lung adenocarcinoma

Antrodia cinnamomea induces anti-tumor activity by inhibiting the STAT3 signaling pathway in lung cancer cells.

Results suggested that STAT3 activity be requisite for the lung tumorigenesis caused by MVP knockdown.

STAT3-induced LINC00668 contributed to non-small cell lung cancer progression through upregulating KLF7 expression by sponging miR-193a.

we found that lung cancer cells induced Adipose-derived mesenchymal stem cells (ADSCs) to secrete high levels of IL-6 family cytokines and activate the STAT3 signalling pathway

ARHGAP15 regulates lung cancer cell proliferation and metastasis via the STAT3 pathway.

MiR-124 changes the sensitivity of lung cancer cells to cisplatin through targeting STAT3.

Role of STAT3 in Resistance of Non-small Cell lung cancer

bioinformatics analysis and in vitro experiments indicated that the role of KLF3 in lung cancer metastasis is dependent on the STAT3 signaling pathway. Overall, our data indicated the crucial function of KLF3 in lung cancer metastasis and suggested opportunities to improve the therapy of patients with lung cancer.

Reciprocal regulation of miR-206 and IL-6/STAT3 pathway mediates IL6-induced gefitinib resistance in EGFR-mutant lung cancer cells.

Study discovered a role of EIF3F-STAT3 interaction in the genetic control of cell migration and metastasis in human lung adenocarcinoma. EIF3F promotes lung cancer cell metastasis in vivo by regulating a cluster of 34 metastasis-promoting genes including Snail2. The interaction between EIF3F and STAT3 controlled the EIF3F-mediated increase in Snail2 expression and cellular invasion.

PTPRT epigenetic silencing defines lung cancer with STAT3 activation and can direct STAT3 targeted therapies.

STAT3 enhanced the expression of HER3 through miR-145-5p repression by G9a, indicating that STAT3 is a reliable therapeutic target against epidermal growth factor receptor-tyrosine kinase inhibitors-resistant lung cancers.

miR4500 suppressed the cell proliferation, migration, invasion and promoted apoptosis of the human nonsmall cell lung cancer cell lines A549 and H1975. expression of STAT3 was negatively correlated with miR4500 expression in vivo. miR4500 directly targeted the 3' untranslated region of STAT3.

C-X-C chemokine receptor 2 correlates with unfavorable prognosis and facilitates malignant cell activities via activating JAK2/STAT3 pathway in non-small cell lung cancer.

MicroRNA-130a enhances the killing ability of natural killer cells against non-small cell lung cancer cells by targeting signal transducers and activators of transcription 3.

Unphosphorylated STAT3 in heterochromatin formation and tumor suppression in lung cancer.

Low phosphorylation level of STAT3 is associated with lung adenocarcinoma.

STAT3-induced upregulation of circCCDC66 facilitates the progression of non-small cell lung cancer by targeting miR-33a-5p/KPNA4 axis.

Downregulation of SETD7 promotes migration and invasion of lung cancer cells via JAK2/STAT3 pathway.

Effects of STAT3 polymorphisms and pharmacokinetics on the clinical outcomes of gefitinib treatment in patients with EGFR-mutation positive non-small cell lung cancer.

Effect of malignant-associated pleural effusion on endothelial viability, motility and angiogenesis in lung cancer.

Aryl hydrocarbon receptor mediates Jak2/STAT3 signaling for non-small cell lung cancer stem cell maintenance.

Glutathione Stransferase omega 1 promotes the proliferation, migration and invasion, and inhibits the apoptosis of nonsmall cell lung cancer cells, via the JAK/STAT3 signaling pathway.

Mesenchymal stem cells enhance lung cancer initiation through activation of IL-6/JAK2/STAT3 pathway.

These findings support the concept that persistent activation of Stat3 induces inflammation during lung cancer by promoting myeloid-derived suppressor cells-mediated immune suppression.

Alterations of STAT3, NF-kappaB and downstream associated molecules are critical in the development of lung tumors and can be exploited as possible mechanisms after the exposure

Data indicate that lung signal transducer and activator of transcription 3 (STAT3) had distinct and opposing roles in the initiation and growth of lung cancer.

PRDX6 promotes lung tumor development via its mediated and CCL5-associated activation of the JAK2/STAT3 pathway.

Data indicate a role of interleukin 6 (IL6)/transcription factor STAT3 (STAT3) signaling in maintaining lung homeostasis and suppressing lung cancer induction.

activation of STAT3 in MDSCs and macrophages promoted tumorigenesis through pulmonary recruitment and increased resistance of suppressive cells to CD8(+) T cells, enhancement of cytotoxicity toward CD4(+) and CD8(+) T cells, induction of regulatory T cell (Treg), inhibition of dendritic cells (DC), and polarization of macrophages toward the M2 phenotype.

Small-scale in vivo screening identified several genes, including Cd109, that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 as a critical, pharmacologically targetable effector of CD109-driven lung cancer metastasis

Lewis lung carcinoma cell-derived extracellular vesicles induced myotube atrophy and adipocyte lipolysis via the extracellular IL-6-mediated STAT3 pathway in target cells.