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Poster presentation 1

1327 - Alterations of cellular proliferation, apoptosis and autophagy by cucurbitacin B treatment in colon cancer cells

Date

19 Dec 2015

Session

Poster presentation 1

Presenters

Moltira Promkan

Citation

Annals of Oncology (2015) 26 (suppl_9): 148-152. 10.1093/annonc/mdv533

Authors

M. Promkan1, S. Dakeng2, P. Suebsakwong3, A. Suksamrarn3, P. Patmasiriwat4

Author affiliations

  • 1 Clinical Microscopy, Faculty of Medical Technology, Mahidol University, 73170 - Nakhon Pathom/TH
  • 2 Clinical Microscopy, Faculty of Medical Technology, Mahidol University, 73170 - Nkhon Pathom/TH
  • 3 Faculty Of Science, Ramkhamhaeng University, Bangkok/TH
  • 4 Clinical Microscopy, Faculty of Medical Technology, Mahidol University, Nkhon Pathom/TH
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Resources

Abstract 1327

Aim/Background

Cucurbitacin B, an oxygenated tetracyclic triterpenoid extracted from the Thai medicinal plant Trichosanthes cucumerina L., exhibited strong anti-proliferative effects against breast cancer cells. However, the molecular mechanism is not completely understood, especially in colon cancer. Colon or colorectal cancer is one of the most common and the leading causes of cancer-related deaths worldwide including in Thailand.

Methods

In this study, we explore the effect of cucurbitacin B on colon cancer cells. Caco-2 and SW620 were treated with the cucurbitacin B and determined for the inhibitory effects on the cell proliferation, transwell cell migration and invasion assay and also effected on colony formation. We examine the influence of cucurbitacin B on apoptosis and autophagy in colon cancer cells.

Results

Upon cucurbitacin B treatment, we found it obvious that cucurbitacin B inhibited cellular proliferation, migration, invasion and colony formation by using anchorage independent growth. The result of flow cytometry also showed that cucurbitacin B can induce apoptosis and autophagy.

Conclusions

Our findings suggest that cucurbitacin B is effectively inhibiting colon cancer, Caco-2 and SW620 cells. However, these findings are now under further investigation in other cell types and/or other mechanisms that may contribute to the development of cucurbitacin B to anti-colon cancer agents. This submitted work provides another crucial progression in the result of cucurbitacin B in colon cancer cells. It may lead to the future application of cucurbitacin B for colon cancer therapy.

Clinical trial identification

Disclosure

All authors have declared no conflicts of interest.

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