overexpression appears to be an early event in lung tumorigenesis; may function as a potential biomarker for the development of NSCLC

Depletion of Bcl-2 by an antisense oligonucleotide induces apoptosis accompanied by oxidation and externalization of phosphatidylserine in NCI-H226 lung carcinoma cells

Bcl-2 downregulation has a role in cisplatin resistance in human small cell lung cancer cells

Advanced stage non-small cell lung tumors or tumors with lymph node metastasis were analyzed, a more favorable survival was noted in patients with bcl-2-positive tumors than those with bcl-2-negative tumors.

overexpression does not affect apoptotic pathway triggered by the Fhit protein in lung cancer cell lines

Bcl-2 expression markedly enhanced spontaneous lung metastasis from orthotopically implanted primary tumors.

Significantly higher Bcl-2 levels were associated with advanced lung cancer patients

The expression rate of bcl-2 was relatively high in small cell lung cancer without any prognostic significance.

Increased serum levels of Bcl-2 is associated with advanced stage non-small cell lung cancer

The expression of p53, Bcl-2 and Bax was altered in lung cancer tissue compared to histologically normal bronchial epithelium.

BCL2 repression by the tumor suppressor activity of the lysyl oxidase propeptide inhibits transformed phenotype of lung and pancreatic cancer cells

p53 and Ki-67, but not bcl-2, cyclin D1 or HER-2 may have roles in the process of tumor genesis in non-small cell lung carcinoma

contributes to drug resistance in small cell lung carcinoma

bcl-2 expression is prognostic for improved oversal survival and disease-specific survival in non-small cell lung carcinoma (NSCLC).

expression predicts chemoradiotherapy outcome in non-small cell lung cancer patients

Upregulation of survivin in non-small cell lung cancer is associated with its neoplasm staging and correlated with p53 and Bcl-2 level.

Bcl-2 expression defines a subgroup of patients with a favorable outcome and may be useful for prognostic stratification of non-small cell lung cancer patients.

ARTN increased BCL2 expression by transcriptional upregulation, and inhibition of BCL2 abrogated the oncogenic properties of ARTN in non-small cell lung carcinoma cells.

High Bcl-2 is associated with squamous cell carcinoma in non-small cell lung cancer.

BCL-2 -938CC genotype is associated with small cell lung cancer

miR-497 could play a role in both gastric and lung cancer cell lines at least in part by modulation of apoptosis via targeting BCL2

Overexpression of BCL-2 is associated with poor response to paclitaxel-based lung cancer chemoradiation.

Angiopoietin-2, an angiogenic regulator, promotes initial growth and survival of breast cancer metastases to the lung through the integrin-linked kinase (ILK)-AKT-B cell lymphoma 2 (Bcl-2) pathway.

The expression of PHD genes and their relationship with the tumor behavior and apoptosis-associated factors in non-small cell lung cancer, was investigated.

non-small cell lung cancer cells were protected from apoptosis through increasing Bag3 expression and consequently promoted the expression of Bcl-XL and Bcl-2.

The increased expression of Bcl-2 is not induced by viral LMP1 in lung cancer patients.

survivin and Bcl-2 may act synergistically in the occurrence, development, invasion and metastasis of non-small cell lung carcinoma (NSCLC), both of which are up-regulated in NSCLC tissues

the novel and multifunctional role of Bcl-2 in malignant transformation and tumorigenesis of human lung epithelial cells chronically exposed to Cr(VI)

Negative expression of Bcl-2 is associated with stage I non-small cell lung cancer.

In non-small cell lung carcinomas, Bcl-2 protein plays an important role in the autophagic process.

The detected Merkel cell polyomavirus (prevalence in non-small cell lung cancer in combination with the deregulated expression of BRAF and Bcl-2 genes suggests that these events are likely to contribute to the pathogenesis of non-small cell lung cancer.

Bcl-2 overexpression induced up-regulation of the proapoptotic protein Bim in lung cancer cells.

Polymorphisms in BCL2 may be associated with survival in advanced-stage non-small cell lung cancer patients who received chemotherapy.

BCL-2 plays a role in the lung cancer drug resistance to the EGFR kinase inhibitors.

miR-503 regulates the resistance of non-small cell lung cancer cells to cisplatin by targeting Bcl-2.

The BCL-2 3'UTR rs1564483A allele was associated with a decreased lung cancer risk and better survival in advanced-stage non-small cell lung cancer male Chinese patients.

High BCL2 expression is associated with small-cell lung cancer.

Studied expression heterogeneity of ITGB3 and BCL-2 in lung adenocarcinoma tissue and adenocarcinoma cell line.

Genetic polymorphism in the inhibitory P2 promoter region of anti-apoptotic BCL-2 genes contributes to the risk of developing non-small-cell lung cancer in Indian population.

the present study demonstrated that waltonitone induced apoptosis of lung cancer cells through, at least partly, miR-663-induced Bcl-2 downregulation.

The findings of the present study provided insight into the molecular mechanisms underlying ferruginol-induced apoptosis in non-small cell lung cancer (NSCLC) cells, indicating that this compound may be a potential candidate drug for anti-NSCLC.

Low expression of Bcl-2 protein is associated with non-small cell lung cancer.

Our results indicate that the BCL-2 rs2279115 genetic variant was associated with small cell lung cancer risk in Chinese populations

Rare bcl-2 overexpression suggests that this anti-apoptotic protein is unlikely to play a role in the apoptotic resistance of non-small cell lung carcinomas.

A decrease in miR-184 level by E6 oncoprotein may predict unfavorable response to cisplatin-based chemotherapy in HPV-infected non-small cell lung carcinoma patients via increasing Bcl-2 expression.

BCL2 expression in mesennchymal lung cancer cells was induced by ERK1 activity through the upregulation of the MEK1/ERK1 scaffold protein MEK partner-1. Interfering with the MEK1/MP1/ERK1 axis using a MEK1 inhibitor or MP1 depletion repressed BCL2 expression and sensitized MLCCs to chemoradiotherapy.

HOTTIP increased the expression of anti-apoptotic factor BCL-2, another important target gene of miR-216a, and jointly enhanced chemoresistance of small cell lung cancer by regulating BCL-2.

Data suggest that circular RNA VANGL1 (circVANGL1) functions as an oncogene to promote non-small cell lung cancer (NSCLC) progression partly through miR-195/BCL2 apoptosis regulator (Bcl-2) axis, which might be a therapeutic target for NSCLC patients.

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.

Antrodia cinnamomea Inhibits Growth and Migration of lung cancer Cells through Regulating p53-Bcl2 and MMPs pathways.