Over-expression of hnRNP A2/B1 is associated with non-small cell lung cancer.

Increased hnRNP A2/B1 expression is associated with non-small cell lung cancer

Detection of plasma hnRNP B1 mRNA by transcription-reverse transcription concerted reaction improves overall prognosis in lung cancer patients.

Neither grade nor stage of non-small cell lung carcinomas was correlated with hnRNP B1 immunreactivity

The positive expression rate of hnRNPA2/B1 in small cell lung cancer was significantly higher than that in the control specimens.

HnRNP A1/A2 and SF2/ASF regulate alternative splicing of interferon regulatory factor-3 and affect immunomodulatory functions in human non-small cell lung cancer cells.

Results demonstrate that by regulating DNA-Protein Kinase activity, hnRNP B1 can affect p53-mediated cell cycle progression and apoptosis, resulting in greater cell survival and subsequent proliferation in human adenocarcinoma of the lungs.

Tissue analysis and knockdown of hnRNPA2B1 using siRNA subsequently demonstrated both the overexpression and potential role for this molecule in lung tumorigenesis.

results demonstrate that hnRNPA2/B1 promotes tumor cell growth by activating COX-2 signaling in NSCLC cells and imply that the hnRNPA2/B1/COX-2 pathway may be a potential therapeutic target for human lung cancers.

Study found that HNRNPA2B1 could be recruited to the 5'UTR of Sp1 mRNA regulating its expression as well as of hnRNPA2B1. Further data indicated that lung cancer patients with higher levels of Sp1 and Nm23-H1 also exhibited high levels of hnRNPA2/B1, suggesting a positive correlation between the levels of Sp1, Nm23-H1 and hnRNPA2B1 during lung cancer formation.