Hypoxia inducible factor-1α promotes cell proliferation and migration in human pancreatic cancer cell line Patu8988
Keywords:
pancreatic cancer, HIF-1α, cell cycle arrest, migration, siRNAAbstract
Aim: Pancreatic cancer cells could survive and proliferate under severe hypoxia, with high expression of hypoxia inducible factor-1α (HIF-1α), which plays a crucial role in cell energy metabolisms, tumor angiogenesis and metastasis in cancer cells. This study investigates the role of HIF-1α on cell proliferation and migration of pancreatic cancer cells. Materials and methods: HIF-1α was knocked down in human pancreatic cancer cell line Patu8988 using siRNA. Cell proliferation was analyzed by MTT assay and cell cycle was analyzed by flow cytometry. Cancer cell mobility was assessed by a migration assay with Boyden chambers. Results: Cell proliferation analysis showed cells with decreased cell growth by MTT assay and G1/S phase cell cycle arrest using flow cytometry. Cancer cell mobility was significantly decreased when the HIF-1α was down-regulated, as assessed by a migration assay with Boyden chambers. Conclusion: These results suggested that down-regulation of HIF-1α could inhibit cell proliferation, and decreased tumor cell migration, which provided a new perspective in understanding the pleiotropic role of HIF-1α in pancreatic cancer.
Downloads
Published
Issue
Section
License
OPEN ACCESS
All the articles of the European Journal of Oncology and Environmental Health are published with open access under the CC-BY Creative Commons attribution license (the current version is CC-BY, version 4.0 http://creativecommons.org/licenses/by/4.0/). This means that the author(s) retain copyright, but the content is free to download, distribute and adapt for commercial or non-commercial purposes, given appropriate attribution to the original article.
The articles in the previous edition of the Journal (European Journal of Oncology) are made available online with open access under the CC-BY Creative Commons attribution license (the current version is CC-BY, version 4.0 http://creativecommons.org/licenses/by/4.0/).
Upon submission, author(s) grant the Journal the license to publish their original unpublished work within one year, and the non exclusive right to display, store, copy and reuse the content. The CC-BY Creative Commons attribution license enables anyone to use the publication freely, given appropriate attribution to the author(s) and citing the Journal as the original publisher. The CC-BY Creative Commons attribution license does not apply to third-party materials that display a copyright notice to prohibit copying. Unless the third-party content is also subject to a CC-BY Creative Commons attribution license, or an equally permissive license, the author(s) must comply with any third-party copyright notices.