Circular RNA circRHOBTB3 inhibits ovarian cancer progression through PI3K/AKT signaling pathway

Author(s):  
Sun Yalan ◽  
Liu Yanfang ◽  
Chen He ◽  
Tan Yujie
2021 ◽  
Vol 11 ◽  
Author(s):  
Limei Yan ◽  
Zeping He ◽  
Wei Li ◽  
Ning Liu ◽  
Song Gao

Ovarian cancer is considered as one of the most fatal gynecologic malignancies. This work aimed to explore the effects and regulatory mechanism of Acyl-CoA medium-chain synthetase-3 (ACSM3, a subunit of CoA ligases) in ovarian cancer progression. As well as employing CCK-8 assay, clone formation assay, and cell cycle analysis were carried out to investigate cell proliferation ability. Wound healing assay and transwell assay were subsequently used to assess cell migration and invasion. Mice xenografts were then conducted to measure the effects of ACSM3 on tumor development in vivo. Our bioinformatics analysis suggested that the expression of ACSM3 was down-regulated in ovarian cancer tissues, and the low expression level of ACSM3 might related with poorer overall survival than high mRNA expression of ACSM3 in ovarian cancer patients. We artificially regulated the expression of ACSM3 to evaluate its effects on ovarian cancer malignant phenotypes. Our data revealed that the overexpression of ACSM3 inhibited cell proliferation, migration, and invasion of ovarian cancer cells. In contrast, the knock-down of ACSM3 received the opposite results. Our western blot results showed that the Integrin β1/AKT signaling pathway was negatively regulated by ACSM3 expression. Moreover, ACSM3 overexpression-induced suppression of cell migration and invasion activities were abolished by the overexpression of ITG β1 (Integrin β1). Additionally, the growth of ovarian cancer xenograft tumors was also repressed by the overexpression of ACSM3. And ACSM3 interference obtained the contrary effects in vivo. In summary, ACSM3 acts as a tumor suppressor gene and may be a potential therapeutic target of ovarian cancer.


2018 ◽  
Vol Volume 11 ◽  
pp. 1333-1343 ◽  
Author(s):  
Biao zeng ◽  
ming zhou ◽  
Huan Wu ◽  
Zhengai Xiong

Life Sciences ◽  
2021 ◽  
Vol 268 ◽  
pp. 118996
Author(s):  
Jiangtao Yu ◽  
Xiaoli Hu ◽  
Xiuxiu Chen ◽  
Qiangyong Zhou ◽  
Qi Jiang ◽  
...  

2019 ◽  
Vol 114 ◽  
pp. 108787 ◽  
Author(s):  
Fan Shen ◽  
Zhi-hong Zong ◽  
Yao Liu ◽  
Shuo Chen ◽  
Xiu-jie Sheng ◽  
...  

2017 ◽  
Vol 50 (5) ◽  
pp. 1601-1611 ◽  
Author(s):  
Benjiang Qian ◽  
Yi Yao ◽  
Changming Liu ◽  
Jiabing Zhang ◽  
Huihong Chen ◽  
...  

2017 ◽  
Vol 16 (3) ◽  
pp. 3600-3605 ◽  
Author(s):  
Jian Cao ◽  
Huiling Li ◽  
Guangquan Liu ◽  
Suping Han ◽  
Pengfei Xu

Author(s):  
Hairul-Islam Ibrahim ◽  
Mohammad Bani Ismail ◽  
Rebai Ben Ammar ◽  
Emad Ahmed

Chemo-resistance and metastatic disease development are the most common causes of breast cancer recurrence and death. Thidiazuron (TDZ) is a plant growth regulator, its biological role on human and animals has not been yet clarified. In the present study, we investigated the anticancer activity of this plant phytohormone on the drug resistant-triple negative breast cancer MDA-MB-231 cell line. Treatment of the breast cancer cells with TDZ (1-50 μM) caused more stressful environment and induced a significant increase in percentages of active caspases positive cells. In addition, TDZ treatment (5 and 10 μM) significantly attenuated the migration and the invasion activities of these highly metastatic cancer cells. Mechanistically, TDZ reducesd cancer progression and invasive activity through targeting miR-202-5p, which stimulatesd the expression of the phosphatase and tensin homolog (PTEN), the tumor suppressor that downregulates PI3K/AKT signaling pathway. In the meantime, TDZ treatment statistically upregulatesd the suppressor of breast cancer proliferation, miRNA-132 that is also implicated in dysregulating the TEN-AKT/the nuclear factor NFκB signaling pathway. Interestingly, our molecular docking analysis revealed potential non-covalent interaction between TDZ with AKT, PTEN and PI3K. These findings suggest that TDZ may suppresses breast cancer metastasis through targeting miRNA-132, miR-202-5p/PTEN and PI3K/AKT downstream molecules.


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