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Luanpitpong S.,Pharmaceutical Technology International Program | Chunhacha P.,Pharmaceutical Technology International Program | Promden W.,Chulalongkorn University | Sriuranpong V.,Chulalongkorn University
Oncology Letters | Year: 2012

Advances in understanding lung cancer biology and tumor markers aid clinicians in managing the disease. Cancer-associated antigen (CA)125 has garnered increasing attention in lung cancer research and may benefit the treatment and follow-up of this type of cancer. In Thai lung cancer patients, knowledge regarding ethnic differences in cancer cell biology is largely absent. We generated lung cancer cells from the pleural effusion fluids of a Thai patient and designated these as P1 cells. P1 cells were assessed for growth rate, response to chemotherapy, and the presence of tumor markers, in particular CA125 expression. Results of immunofluorescence indicated that P1 cells exhibited strong expression levels of CA125, comparable to that of established H460 lung cancer cells. Furthermore, P1 cells were analyzed for the expression of additional markers. Results revealed that H460 cells exhibited strong immunofluorescent signals from cytokeratin-19 fragments (CYFRA 21-1) and squamous cell carcinoma antigen (SCCA) while P1 presented only CYFRA 21-1 signals. We also found evidence of relative cisplatin resistance in P1 compared to the susceptibility level of established lung cancer cells. Thus, the results and methodology described in this study may aid the development of lung cancer diagnostic and therapeutic approaches and, in particular, advance understanding of ethnic differences.

Halim H.,Pharmaceutical Technology International Program | Chunhacha P.,Pharmaceutical Technology International Program | Suwanborirux K.,Chulalongkorn University | Chanvorachote P.,Chulalongkorn University
Anticancer Research | Year: 2011

Background: Renieramycin M, has been shown to exhibit promising anticancer activity against some cancer cell lines; however, the underlying mechanism remains unknown. Materials and Methods: Renieramycin M was isolated from the blue sponge Xestospongia sp. Anticancer and antimetastatic activities of renieramycin M were investigated in human non-small cell lung cancer cells. Results: Renieramycin M treatment caused p53 activation, which subsequently down-regulated anti-apoptotic MCL-1 and BCL-2 proteins, while the level of pro-apoptotic BAX protein was not altered. The subtoxic concentrations of renieramycin M significantly decreased invasion and migration abilities of cancer cells. In addition, this compound showed a strong inhibitory effect on anchorage-independent growth of the cells. Conclusion: These results reveal that renieramycin M induced lung cancer cells apoptosis through p53-dependent pathway and the compound may inhibit progression and metastasis of lung cancer cells.

Chunhacha P.,Pharmaceutical Technology International Program | Pongrakhananon V.,Chulalongkorn University | Rojanasakul Y.,West Virginia University | Chanvorachote P.,Chulalongkorn University
American Journal of Physiology - Cell Physiology | Year: 2012

Both caveolin-1 (Cav-1) and Mcl-1 have been implicated in the regulation of cancer cell anoikis, but their relationship and underlying mechanisms of regulation are not known. The present study demonstrated for the first time that Cav-1 regulates Mcl-1 through protein-protein interaction and inhibits its down regulation during cell anoikis in human lung cancer cells. Immunoprecipitation and immunocyto-chemistry studies showed that Cav-1 interacted with Mcl-1 and prevented it from degradation via the ubiquitin-proteasome pathway. Mcl-1 and Mcl-1-Cav-1 complex were highly elevated in Cav-1-overexpressing cells but were greatly reduced in Cav-1 knockdown cells. Consistent with this finding, we found that Mcl-1 ubiquitination was significantly attenuated by Cav-1 over expression but increased by Cav-1 knockdown. Together, our results indicate a novel role of Cav-1 in anoikis regulation through Mcl-1 interaction and stabilization, which provides a new insight to the pathogenesis of metastatic lung cancer and its potential treatment. © 2012 the American Physiological Society.

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