Unknown

Dataset Information

0

Gelsolin regulates proliferation, apoptosis and invasion in natural killer/T-cell lymphoma cells.


ABSTRACT: The expression of gelsolin (GSN) is abnormal in many cancers, including extranodal nasal-type natural killer/T-cell lymphoma (NKTCL). However, the biological function of GSN and its mechanism in NKTCL remain unclear. We found that GSN overexpression significantly suppressed cell proliferation, colony formation and invasion, and promoted apoptosis of natural killer (NK) cell line YTS. Moreover, the upregulation of GSN significantly decreased the levels of PI3K and p-Akt. Interestingly, blocking the PI3K/Akt signaling pathway significantly inhibited cell proliferation and invasion and promoted apoptosis of YTS cells. In conclusion, our findings indicate that GSN can suppress cell proliferation and invasion and promote apoptosis of YTS cells, and the PI3K/Akt signaling pathway is likely to be involved in this process.

SUBMITTER: Guo Y 

PROVIDER: S-EPMC5827263 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

altmetric image

Publications

Gelsolin regulates proliferation, apoptosis and invasion in natural killer/T-cell lymphoma cells.

Guo Yanwei Y   Zhang Hongqiao H   Xing Xin X   Wang Lijuan L   Zhang Jian J   Yan Lin L   Zheng Xiaoke X   Zhang Mingzhi M  

Biology open 20180117 1


The expression of gelsolin (GSN) is abnormal in many cancers, including extranodal nasal-type natural killer/T-cell lymphoma (NKTCL). However, the biological function of GSN and its mechanism in NKTCL remain unclear. We found that GSN overexpression significantly suppressed cell proliferation, colony formation and invasion, and promoted apoptosis of natural killer (NK) cell line YTS. Moreover, the upregulation of GSN significantly decreased the levels of PI3K and p-Akt. Interestingly, blocking t  ...[more]

Similar Datasets

| S-EPMC4801461 | biostudies-literature
| S-EPMC5884382 | biostudies-literature
| S-EPMC5446977 | biostudies-literature
| S-EPMC6527808 | biostudies-literature
| S-EPMC7877170 | biostudies-literature
| S-EPMC6628536 | biostudies-literature
| S-EPMC6277620 | biostudies-literature
| S-EPMC4980213 | biostudies-other
| S-EPMC4921106 | biostudies-literature
| S-EPMC6280527 | biostudies-literature