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Mechanism of RNA Binding Protein Sam68 Regulating Biological Behavior of Gastric Cancer Cells and Prognosis of Patients / 胃肠病学
Chinese Journal of Gastroenterology ; (12): 348-352, 2021.
Artículo en Chino | WPRIM | ID: wpr-1016214
ABSTRACT

Background:

The dysregulation of expression of Sam68 gene can induce cell cycle progression, cell proliferation, transformation, tumorigenesis, and metastasis of multiple types of cancer cells. However, the specific role and molecular mechanism of Sam68 in gastric cancer cells are still uncertain.

Aims:

To investigate the correlation of expression of Sam68 with prognosis of gastric cancer patients and biological behavior of gastric cancer cells.

Methods:

A total of 161 gastric cancer tissue and paracancerous normal tissue specimens were collected. Western blotting and immunohistochemical staining were used to detect the expression of Sam68, and its correlations with clinicopathological features were analyzed. Gastric cancer AGS cells were transfected by siRNA Sam68. Cell proliferation was evaluated by CCK-8 assay, cell migration ability was evaluated by scratch test, and cell invasion ability was evaluated by Transwell test.

Results:

Expression of Sam68 was increased in gastric cancer tissue, and was correlated with depth of infiltration, TNM staging and lymph node metastasis. The high expression of Sam68 was correlated with poor prognosis of gastric cancer patients. After transfection with Sam68 siRNA, cell proliferation, cell cycle progression, migration and invasion ability were decreased.

Conclusions:

Sam68 may be a new factor for the growth, migration and invasion of gastric cancer cells, and has significant value in predicting the prognosis of gastric cancer patients.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Gastroenterology Año: 2021 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Gastroenterology Año: 2021 Tipo del documento: Artículo