BMC Cancer,2021年
Hongfei Liu, Jie Sun, Zheng Dong, Xiaodong Jia, Dawei Wu, Aaron Ge, Yinying Lu, Shanshan Lu, Deyuan Zhang, Zhengyao Chang, Pan Zhao, Qiyu Jiang, Jing Wang
LicenseType:CC BY |
BMC Cancer,2021年
Jing Wang, Liling Huang, Shiyu Jiang, Zhihuang Hu, Hongnan Zhen, Peijie Jin
LicenseType:CC BY |
BMC Cancer,2021年
Anastasiia Leonteva, Jing Wang, Chuang Nie, Jia Hong, Xu Han, Lin Zhu, Yashuang Zhao, Xinyu Du, Haibo Zhou, Wenjing Tian, Rongrong Wei, Yingwei Xue
LicenseType:CC BY |
4 PCAF-mediated acetylation of Lin28B increases let-7 biogenesis in lung adenocarcinoma H1299 cells [期刊论文]
BMC Cancer,2018年
Yan-jun Zhang, Fei Chen, Ting-ting Qu, Wen-zheng Sun, Ye Zhang, Jing Wang, Yu-fei Shen, Mo-bin Cheng
LicenseType:Unknown |
5 Transforming growth factor-β suppresses metastasis in a subset of human colon carcinoma cells [期刊论文]
BMC Cancer,2012年
Michael G Brattain, Jing Wang, Carol A Teggart, Melanie Ongchin, Elizabeth A Sharratt, Ashwani Rajput, Neka AKSimms
英文
Background
TGFβ signaling has typically been associated with suppression of tumor initiation while the role it plays in metastasis is generally associated with progression of malignancy. However, we present evidence here for an anti-metastatic role of TGFβ signaling.
Methods
To test the importance of TGFβ signaling to cell survival and metastasis we compared human colon carcinoma cell lines that are either non-tumorigenic with TGFβ response (FET), or tumorigenic with TGFβ response (FETα) or tumorigenic with abrogated TGFβ response via introduction of dominant negative TGFβRII (FETα/DN) and their ability to metastasize. Metastatic competency was assessed by orthotopic transplantation. Metastatic colony formation was assessed histologically and by imaging.
Results
Abrogation of TGFβ signaling through introduction of a dominant negative TGFβ receptor II (TGFβRII) in non-metastatic FETα human colon cancer cells permits metastasis to distal organs, but importantly does not reduce invasive behavior at the primary site. Loss of TGFβ signaling in FETα-DN cells generated enhanced cell survival capabilities in response to cellular stress in vitro. We show that enhanced cellular survival is associated with increased AKT phosphorylation and cytoplasmic expression of inhibitor of apoptosis (IAP) family members (survivin and XIAP) that elicit a cytoprotective effect through inhibition of caspases in response to stress. To confirm that TGFβ signaling is a metastasis suppressor, we rescued TGFβ signaling in CBS metastatic colon cancer cells that had lost TGFβ receptor expression due to epigenetic repression. Restoration of TGFβ signaling resulted in the inhibition of metastatic colony formation in distal organs by these cells. These results indicate that TGFβ signaling has an important role in the suppression of metastatic potential in tumors that have already progressed to the stage of an invasive carcinoma.
Conclusions
The observations presented here indicate a metastasis suppressor role for TGFβ signaling in human colon cancer cells. This raises the concern that therapies targeting inhibition of TGFβ signaling may be imprudent in some patient populations with residual TGFβ tumor suppressor activity.
BMC Cancer,2014年
Yi-Sheng Zhong, Bing Xie, Zi-Jian Yang, Xiao-Hong Liu, Jing Wang
英文
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Background
Retinoblastoma (Rb) is the most common intraocular tumor in childhood worldwide. It is a deadly pediatric eye cancer. The main cause of death in Rb patients is intracranial and systemic metastasis. ROCK is the main downstream effector of Ras-homologous (Rho) family of GTPases which are involved in many cellular functions, such as cell proliferation, invasion and metastasis. Overexpression of ROCK promotes invasion and metastasis of many solid tumors. However, the effect of ROCK in Rb is largely unknown.
Methods
ROCK-1 and ROCK-2 mRNA expression in Y79 cell lines were examined by RT-PCR. Protein expression in the Y79 cell line were examined by western blot analyses. ROCK-1 and ROCK-2 siRNA were transfected into Y79 cells with Lipofectamine 2000. Cell proliferation was evaluated by CCK-8 assay after exposure to ROCK inhibitor (Y-27632). We examined the effect of ROCK inhibitors (Y-27632, ROCK-1 and ROCK-2 siRNA) on Y79 cell adhesive capacity by cell adhesion assay. Cell invasion assay through matrigel was used to study the effect of ROCK inhibitors on Y79 cell invasive capacity.
Results
The expression of mRNA of ROCK-1 was more than that of ROCK-2 in the Y79 cell line. The protein expression levels of ROCK-1 and ROCK-2 were downregulated in the cells transfected with siRNA. Y-27632 treatment didn’t lead to any changes of Y79 cells proliferation. Adhesive ability of Y79 cells was enhanced following Y-27632 or ROCK-1 siRNA treatment. The invasive capacity of Y79 cells showed an inverse relationship with increasing Y-27632 concentration. Invasiveness of Y79 cells also decreased in Y79 cells transfected with ROCK-1 siRNA. However, there was no change in adhesive ability or invasive capacity in Y79 cells transfected with siRNA against ROCK-2.
Conclusions
The findings of this study demonstrate that ROCK-1 protein plays a key role in regulating metastasis and invasion of Y79 cells, suggesting that the ROCK-1 dependent pathway may be a potential target for therapy of Rb.
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