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S. Kumar
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P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P1.04-080 - miR-326 Is Down-Regulated in Non-Small Cell Lung Cancer and Targets NFIB, a Lung Developmental Gene: A Pilot Study (ID 1326)
09:30 - 09:30 | Author(s): S. Kumar
- Abstract
Background:
Lung cancer is the leading cause of cancer mortality worldwide. Non-small cell lung cancer (NSCLC) is the most common subtype, accounting for about 80% of all lung cancers. miRNAs are small RNAs of 21-24 nucleotides in length, which play major role in cell proliferation and differentiation and their differential expression is known to be associated with various cancers including lung cancer. Role of miR-326 has been previously studied as a marker of bone metastasis in lung cancer. Moreover, we have previously shown that miR-326 plays a critical role in the epithelial to mesenchymal transition (EMT) by targeting transforming growth factor (TGF)-β1 and other members of TGF-β signaling pathway. The aim of present study is to check the expression and correlation of miR-326 and lung epithelial developmental gene nuclear factor IB (NFIB) in non-small cell lung cancer tissue samples as cancer metastasis is accompanied by EMT.
Methods:
We have examined eight pathologically confirmed non-small cell lung cancer cases. All patients were men and smokers with age ranged from 29 to 74 years (mean 54.6 years). Surgical resection was performed in all the cases which were either stage II or III. Histopathologically, 4 cases were squamous cell carcinomas, 3 were adenocarcinomas including one case of invasive mucinous carcinoma and one case was low grade mucoepidermoid carcinoma. RNA was isolated from fresh frozen tissue to check for miR-326 and NFIB levels by real time PCR. Protein expression was checked by immunohistochemistry (NFIB; 1:200; Abcam)) and in-situ hybridization (miR-326; Exiqon). Adjoining lung tissue served as normal control in each case.
Results:
Expression of both miR-326 and NFIB was found to be down regulated in non-small cell lung cancer tissue at both RNA and protein level (Fig 1A-C). Our in silico experiments identified a target site of miR-326 at the 3’UTR of NFIB gene; presumably it stabilizes the transcripts of NFIB (Fig 1D). Figure 1
Conclusion:
Our preliminary data suggests that miR-326 stabilizes the transcripts of NFIB in normal epithelial cells and maintain epithelial cell integrity. Dysregulation of miR-326 and NFIB in non-small cell lung cancer indicate that miR-326 and NFIB work synergistically and may contribute to the development of non-small cell lung cancer.
