Knockdown of RAB25 promotes autophagy and inhibits cell growth in ovarian cancer cells

被引：34
|
作者：
Liu, Yingtao
Tao, Xiang
Jia, Luoqi
Cheng, Kwai Wa [2 ]
Lu, Yiling [2 ]
Yu, Yinhua
Feng, Youji [1 ,3 ]
机构：
[1] Fudan Univ, Obstet & Gynecol Hosp, Dept Gynecol, Shanghai 200011, Peoples R China
[2] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77054 USA
[3] Jiao Tong Univ, Shanghai Peoples Hosp 1, Dept Obstet & Gynecol, Shanghai 200080, Peoples R China
来源：
MOLECULAR MEDICINE REPORTS | 2012年 / 6卷 / 05期
基金：
中国国家自然科学基金;
关键词：
RAB25; ovarian cancer; autophagy; extracellular signal-regulated kinases; proliferation; apoptosis; DEATH; EXPRESSION; SURVIVAL; IDENTIFICATION; TUMORIGENESIS; CARCINOMA; APOPTOSIS; BINDING; PROTEIN; ERK1/2;
D O I：
10.3892/mmr.2012.1052
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
RAB25 belongs to the Rab family of small GTPases and is implicated in the development of various types of human cancer. To evaluate the role of RAB25 in ovarian cancer, RAB25 was knocked down by siRNA in HEY and ES-2 human ovarian cancer cells. Autophagy, cell growth and cell apoptosis were evaluated. The results showed that knockdown of RAB25 increased acidic vesicle organelles and GFP-microtubule-associated protein 1 light chain 3 punctate fluorescence in ovarian cancer cells. Autophagy that promoted by knockdown of RAB25 was not observed in cells where the ERK1/2 signaling pathway had been inhibited by U0126. Knockdown of RAB25 reduced cell cycle progression and cell growth. Apoptosis of ovarian cancer cells could be induced by knockdown of RAB25. These results support the tumorigenic role of RAB25 in ovarian cancer cells.
引用
收藏
页码：1006 / 1012
页数：7
相关论文
共 50 条
  • [1] Knockdown of Rab25 expression by RNAi inhibits growth of human epithelial ovarian cancer cells in vitro and in vivo
    Fan Yang
    Xin Xiao-Yan
    Chen Bi-Liang
    Ma Xiangdong
    PATHOLOGY, 2006, 38 (06) : 561 - 567
  • [2] Follicle-stimulating hormone inhibits apoptosis and autophagy in ovarian cancer cells by activating survivin and Rab25
    Liu, Yingtao
    Huang, Yan
    Jin, Hongyan
    Cheng, Kwai Wa
    Lu, Yiling
    Yu, Yinhua
    Feng, Youji
    CANCER RESEARCH, 2010, 70
  • [3] Follicle-stimulating hormone inhibits apoptosis and autophagy in ovarian cancer cells by activating survivin and Rab25
    Liu, Yingtao
    Huang, Yan
    Jin, Hongyan
    Cheng, Kwai Wa
    Lu, Yiling
    Yu, Yinhua
    Feng, Youji
    CANCER RESEARCH, 2010, 70
  • [4] Overexpression of Rab25 promotes hepatocellular carcinoma cell proliferation and invasion
    Geng, Donghua
    Zhao, Wenyan
    Feng, Yong
    Liu, Jingang
    TUMOR BIOLOGY, 2016, 37 (06) : 7713 - 7718
  • [5] Loss of Rab25 promotes intestinal neoplasia
    Nam, Ki-Taek
    Lee, Hyuk-Joon
    Coffey, Robert J.
    Yeatman, Timothy J.
    Aronow, Bruce J.
    Goldenring, James R.
    GASTROENTEROLOGY, 2008, 134 (04) : A305 - A305
  • [6] RAB25 confers resistance to chemotherapy by altering mitochondrial apoptosis signaling in ovarian cancer cells
    Sehime Gulsun Temel
    Aslı Giray
    Bahriye Karakas
    Ozgur Gul
    Ilknur Kozanoglu
    Husnu Celik
    Huveyda Basaga
    Ufuk Acikbas
    Ceren Sucularli
    Sidika Oztop
    Yeliz Aka
    Ozgur Kutuk
    Apoptosis, 2020, 25 : 799 - 816
  • [7] Rab25 in cancer: a brief update
    Mitra, Shreya
    Cheng, Kwai W.
    Mills, Gordon B.
    BIOCHEMICAL SOCIETY TRANSACTIONS, 2012, 40 : 1404 - 1408
  • [8] Rab25 and RCP in cancer progression
    Kyung Hwa Cho
    Hoi Young Lee
    Archives of Pharmacal Research, 2019, 42 : 101 - 112
  • [9] Rab25 and RCP in cancer progression
    Cho, Kyung Hwa
    Lee, Hoi Young
    ARCHIVES OF PHARMACAL RESEARCH, 2019, 42 (02) : 101 - 112
  • [10] RAB25 confers resistance to chemotherapy by altering mitochondrial apoptosis signaling in ovarian cancer cells
    Temel, Sehime Gulsun
    Giray, Asli
    Karakas, Bahriye
    Gul, Ozgur
    Kozanoglu, Ilknur
    Celik, Husnu
    Basaga, Huveyda
    Acikbas, Ufuk
    Sucularli, Ceren
    Oztop, Sidika
    Aka, Yeliz
    Kutuk, Ozgur
    APOPTOSIS, 2020, 25 (11-12) : 799 - 816
12345