The interplay between HPIP and casein kinase 1α promotes renal cell carcinoma growth and metastasis via activation of mTOR pathway

Mai, Haixing; Xu, Xiaowei; Guo-Hui, Mei; Hong, Tian; Huang, Jun; Wang, T; Zhang, Yan; Li, Y; Liang, Yingchun; Li, L; Jin, Shuai; You, Wenye; Ma, Yue; L, Chen; Ye, Qianli

doi:10.1038/oncsis.2016.44

Cited by 19 publications

(19 citation statements)

References 30 publications

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“…High mTOR protein expression levels have been detected in non-small cell lung cancer (NSCLC) tissues and cell lines, and suppressing mTOR could attenuate the development of cancer [30]. Deactivating the mTOR pathway also inhibits cancer metastasis and invasion [31]. A recent study proposed that miR-496 negatively regulated mTOR by targeting two sites within its 3 0 -UTR [19].…”

Section: Discussionmentioning

confidence: 99%

LncRNA‐DANCR contributes to lung adenocarcinoma progression by sponging miR‐496 to modulate mTOR expression

Rui

Guo

et al. 2017

J Cellular Molecular Medi

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Long non‐coding RNAs (lncRNAs) have emerged as new and important regulators of pathological processes including tumour development. In this study, we demonstrated that differentiation antagonizing non‐protein coding RNA (DANCR) was up‐regulated in lung adenocarcinoma (ADC) and that the knockdown of DANCR inhibited tumour cell proliferation, migration and invasion and restored cell apoptosis rescued; cotransfection with a miR‐496 inhibitor reversed these effects. Luciferase reporter assays showed that miR‐496 directly modulated DANCR; additionally, we used RNA‐binding protein immunoprecipitation (RIP) and RNA pull‐down assays to further confirm that the suppression of DANCR by miR‐496 was RISC‐dependent. Our study also indicated that mTOR was a target of miR‐496 and that DANCR could modulate the expression levels of mTOR by working as a competing endogenous RNA (ceRNA). Furthermore, the knockdown of DANCR reduced tumour volumes in vivo compared with those of the control group. In conclusion, this study showed that DANCR might be an oncogenic lncRNA that regulates mTOR expression through directly binding to miR‐496. DANCR may be regarded as a biomarker or therapeutic target for ADC.

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Section: Discussionmentioning

confidence: 99%

LncRNA‐DANCR contributes to lung adenocarcinoma progression by sponging miR‐496 to modulate mTOR expression

Rui

Guo

et al. 2017

J Cellular Molecular Medi

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“…The ERK/RSK1 pathway plays a critical role in determining the response of RCC cells to mTOR inhibitors via regulating hypoxia‐inducible factor 2α/p21 . The mTOR pathway has been reported to be implicated in promoting RCC growth and metastasis . In addition, Yang et al .…”

Section: Discussionmentioning

confidence: 99%

Retracted: Ubiquitin ligase SMURF1 functions as a prognostic marker and promotes growth and metastasis of clear cell renal cell carcinoma

et al. 2017

FEBS Open Bio

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Smad ubiquitin regulatory factor 1 (SMURF1), a recently identified E3 ubiquitin ligase, targets substrate proteins for ubiquitination and proteasomal degradation. Previous studies have reported that SMURF1 also functions as an oncogene in human cancers. However, the clinical value of SMURF1 and its role in clear cell renal cell carcinoma (ccRCC) are unknown. SMURF1 expression was analyzed in 100 cases of ccRCC and matched tumor‐adjacent specimens. SMURF1 was prominently overexpressed in ccRCC specimens compared with tumor‐adjacent specimens. Increased levels of SMURF1 were also observed in ccRCC cell lines. Clinicopathological detection verified that SMURF1 expression was associated with advanced tumor node metastasis stage, large tumor size and vascular invasion of ccRCC patients. Moreover, Kaplan–Meier analysis found that SMURF1 elevation led to adverse overall survival and disease‐free survival. Multivariate Cox regression analysis revealed that SMURF1 expression was an independent marker for prognosis prediction. Further experiments illustrated that SMURF1 knockdown significantly inhibited growth and metastasis of 769P cells, while SMURF1 overexpression promoted proliferation, migration and invasion in OSRC‐2 cells. Mechanistically, SMURF1 inversely regulated the expression of DAB2 interacting protein, which negatively mediated the activation of both the ERK/RSK1 and PI3K/AKT/mTOR pathways in ccRCC cells. Taken together, these results suggest that SMURF1 might be a promising biomarker and target for novel treatment of human ccRCC.

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“…In current EAU guidelines on RCC, molecular factor as a prognostic factor is clear (3). In recent years, more and more important genes were discovered on RCC, such as Polybromo-1 (PBRM1) (12), Von Hippel-Lindau (VHL) (13), Mammalian Target of Rapamycin (mTOR) (14) and so on. PBRM1 is the second major RCC gene, with truncating mutations in 41% of cases.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic miR-23a-5p is associated with cellular function in RCC

Quan

Jin

Pan

et al. 2017

Molecular Medicine Reports

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In recent years, accumulating evidence has demonstrated that microRNAs (miRs, miRNAs) may serve an important role in the occurrence and development of tumors. miR‑23a‑5p has been confirmed as an oncogene in numerous diseases through gene chip analysis. However, as the most common type of renal tumor, the expression and function of miR‑23a‑5p in renal cell carcinoma (RCC) remains unclear. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis, and Cell Counting Kit‑8 (CCK‑8), wound scratch, Transwell, MTT and flow cytometry assays were performed to investigate the role of miR‑23a‑5p in RCC. The expression of miR‑23a‑5p in RCC tissue samples was significantly higher compared with that in normal tissue samples (P<0.01). Furthermore, the expression of miR‑23a‑5p in RCC cell lines (786O, ACHN and Caki‑1) was significantly higher compared with that in the human embryo kidney 293T cell line, as determined using RT‑qPCR (P<0.001). In addition, the results revealed that the upregulation of miR‑23a‑5p promoted the proliferation, migration and invasion of RCC cells, and inhibited RCC cell apoptosis. The downregulation of miR‑23a‑5p resulted in the reversal of the results described above. Additionally, it was observed that the downregulation of miR‑23a‑5p significantly promoted ACHN and 786O cell viability (P<0.001). The results of the present study suggest that miR-23a-5p is an oncogene in the occurrence and development of RCC and may be a novel therapeutic target for RCC.

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The interplay between HPIP and casein kinase 1α promotes renal cell carcinoma growth and metastasis via activation of mTOR pathway

Cited by 19 publications

References 30 publications

LncRNA‐DANCR contributes to lung adenocarcinoma progression by sponging miR‐496 to modulate mTOR expression

LncRNA‐DANCR contributes to lung adenocarcinoma progression by sponging miR‐496 to modulate mTOR expression

Retracted: Ubiquitin ligase SMURF1 functions as a prognostic marker and promotes growth and metastasis of clear cell renal cell carcinoma

Oncogenic miR-23a-5p is associated with cellular function in RCC

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