scholarly journals Tumor-suppressivemicroRNA-135ainhibits cancer cell proliferation by targeting thec-MYConcogene in renal cell carcinoma

2012 ◽  
Vol 104 (3) ◽  
pp. 304-312 ◽  
Author(s):  
Yasutoshi Yamada ◽  
Hideo Hidaka ◽  
Naohiko Seki ◽  
Hirofumi Yoshino ◽  
Takeshi Yamasaki ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Cancer Cell Proliferation

The expression of Cullin1 is increased in renal cell carcinoma and promotes cancer cell proliferation, migration, and invasion

Tumor Biology ◽  
2016 ◽  
Vol 37 (9) ◽  
pp. 12823-12831 ◽  
Author(s):  
Ji-Gen Ping ◽  
Fei Wang ◽  
Jin-Xian Pu ◽  
Ping-Fu Hou ◽  
Yan-Su Chen ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation

scholarly journals Endocytosis-Mediated Replenishment of Amino Acids Favors Cancer Cell Proliferation and Survival in Chromophobe Renal Cell Carcinoma

2020 ◽  
Vol 80 (24) ◽  
pp. 5491-5501
Author(s):  
Yi Xiao ◽  
Anja Rabien ◽  
René Buschow ◽  
Vyacheslav Amtislavskiy ◽  
Jonas Busch ◽  
...  
Keyword(s):  
Amino Acids ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Chromophobe Renal Cell Carcinoma ◽  
Cancer Cell Proliferation

464 TUMOR-SUPPRESSIVE MIR-135A INHIBITS CANCER CELL PROLIFERATION BY TARGETING THE C-MYC ONCOGENE IN RENAL CELL CARCINOMA

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Hideo Hidaka ◽  
Hirohumi Yoshino ◽  
Hideki Enokida ◽  
Takeshi Yamasaki ◽  
Toshihiko Itesako ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Cancer Cell ◽  
Renal Cell ◽  
Cancer Cell Proliferation ◽  
Myc Oncogene

scholarly journals LncRNA POU3F3 Promotes Cancer Cell Proliferation, Migration, and Invasion in Renal Cell Carcinoma by Downregulating LncRNA GAS5

2021 ◽  
pp. 1-7
Author(s):  
Lei Zhang ◽  
Cezheng Wang ◽  
Min Ma
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
In Situ Hybridization ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Tumor Tissues ◽  
Lncrna Gas5

<b><i>Background:</i></b> LncRNAs play regulatory roles in diverse nephrological disorders, including renal cancer. Overexpression of lncRNA POU3F3 (POU3F3) has only been reported in esophageal squamous-cell carcinomas, indicating POU3F3 may be an oncogene in this disease. LncRNA GAS5 (GAS5) was reported to be a suppressor in various tumors. However, the roles and underlying mechanism of POU3F3 and GAS5 involved in renal cell carcinoma (RCC) remain unknown. <b><i>Methods:</i></b> Real-time quantitative PCR and in situ hybridization were performed to determine the expression of POU3F3 and GAS5 in paired tumor and adjacent healthy tissues donated by 68 RCC patients. The prognostic values of POU3F3 and GAS5 for RCC were analyzed by performing a 5-year follow-up study. Overexpression of POU3F3 and GAS5 was achieved in RCC cells to explore the interactions between them. Transwell assay and cell proliferation assay were performed to evaluate the role of POU3F3 and GAS5 in regulating RCC cell proliferation, migration, and invasion. <b><i>Results:</i></b> In the present study, we found that POU3F3 was upregulated while GAS5 was downregulated in tumor tissues than that in adjacent healthy tissues of patients with RCC. In situ hybridization analysis showed that POU3F3 was mostly expressed in tumor tissues, while GAS5 was mostly expressed in adjacent healthy tissues. High level of POU3F3 and low level of GAS5 were closely correlated with poor prognosis of RCC patients. Expression levels of POU3F3 and GAS5 were significantly and inversely correlated in tumor tissues but not in adjacent healthy tissues of RCC patients. Overexpression of POU3F3 mediated the downregulation of GAS5 in RCC cells, while GAS5 overexpression failed to significantly affect POU3F3 expression. Overexpression of POU3F3 led to promoted, while GAS5 overexpression led to inhibited proliferation, migration, and invasion of RCC cells. In addition, GAS5 overexpression attenuated the enhancing effects of POU3F3 overexpression on cancer cell proliferation, migration, and invasion. <b><i>Conclusion:</i></b> POU3F3 promoted cell proliferation, migration, and invasion in RCC possibly by downregulating GAS5.

scholarly journals Mechanistic Target of Rapamycin Inhibitors in Renal Cell Carcinoma: Potential, Limitations, and Perspectives

2021 ◽  
Vol 9 ◽  
Author(s):  
Seraina Faes ◽  
Nicolas Demartines ◽  
Olivier Dormond
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Mtor Inhibitors ◽  
Target Of Rapamycin ◽  
Cancer Cell Proliferation ◽  
Hypoxia Inducible Factors ◽  
Mtor Signaling Pathway ◽  
Mechanistic Target Of Rapamycin

Several elements highlight the importance of the mechanistic target of rapamycin (mTOR) in the biology of renal cell carcinoma (RCC). mTOR signaling pathway is indeed frequently activated in RCC, inducing cancer cell proliferation and survival. In addition, mTOR promotes tumor angiogenesis and regulates the expression of hypoxia-inducible factors that play an important role in a subset of RCC. Despite mTOR protumorigenic effects, mTOR inhibitors have failed to provide long-lasting anticancer benefits in RCC patients, highlighting the need to readdress their role in the treatment of RCC. This review aims to present the rationale and limitations of targeting mTOR in RCC. Future roles of mTOR inhibitors in the treatment of RCC are also discussed, in particular in the context of immunotherapies.

TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Lymphatic Invasion ◽  
Cancer Specific Survival ◽  
Candidate Target ◽  
Candidate Target Gene ◽  
And Migration

TRIM44 has oncogenic roles in various cancers. However, TRIM44 expression andits function in renal cell carcinoma (RCC) are still unknown. Here in this study, weinvestigated the clinical significance of TRIM44 and its biological function in RCC.TRIM44 overexpression was significantly associated with clinical M stage, histologictype (clear cell) and presence of lymphatic invasion (P = .047, P = .005, and P = .028,respectively). Moreover, TRIM44 overexpression was significantly associated withpoor prognosis in terms of cancer-specific survival (P = .019). Gain-of-function andloss-of-function studies using TRIM44 and siTRIM44 transfection showed thatTRIM44 promotes cell proliferation and cell migration in two RCC cell lines, Caki1and 769P. To further investigate the role of TRIM44 in RCC, we performed integratedmicroarray analysis in Caki1 and 769P cells and explored the data in the Oncominedatabase. Interestingly, FRK was identified as a promising candidate target gene ofTRIM44, which was downregulated in RCC compared with normal renal tissues. Wefound that cell proliferation was inhibited by TRIM44 knockdown and then recoveredby siFRK treatment. Taken together, the present study revealed the associationbetween high expression of TRIM44 and poor prognosis in

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