MicroRNA‑218 inhibits the cell proliferation and migration in clear cell renal cell carcinoma through targeting cancerous inhibitor of protein phosphatase 2A

Wei, Ruojing; Ye, Xiongjun; Zhao, Yawei; Jia, Ning; Liu, Tongwei; Lian, Wenfeng; Wei, Hong-Jian; Zhang, Gang; Song, Lijie

doi:10.3892/ol.2019.9986

Cited by 10 publications

(8 citation statements)

References 22 publications

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“…ccRCC is characterized by high invasiveness, high mortality, and resistance to conventional treatment regimens including chemotherapy and radiation [21,22]. In addition, most ccRCC patients are already in the advanced stage at diagnosis, and there are currently no biomarkers for early diagnosis or treatment of ccRCC [23], resulting in a relatively poor prognosis for ccRCC [24]. Therefore, it is necessary to understand the mechanism behind the initiation of metastasis in ccRCC and to find effective therapeutic targets for treating metastatic ccRCC [21].…”

Section: Discussionmentioning

confidence: 99%

TNFAIP8 promotes the migration of clear cell renal cell carcinoma by regulating the EMT

Zhong¹,

Zhu²,

Liu³

et al. 2020

J. Cancer

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Background: Clear cell renal cell carcinoma (ccRCC) is characterized by high metastatic potential, and the epithelial-mesenchymal transition (EMT) has been shown to play a key role in multiple cancer progression, migration and metastasis and is the leading cause of poor prognosis. Currently, tumor necrosis factor-α-induced protein 8 (TNFAIP8/TIPE) is a newly discovered tumorigenesis factor, and TNFAIP8 and the EMT influence the migration of renal cancer cells. Methods: In this study, we first analyzed the relationship between TNFAIP8 and ccRCC using bioinformatics, followed by immunohistochemistry to evaluate the relationship between the two in clinical samples. Subsequently, reverse transcription PCR and western blotting confirmed the expression of TNFAIP8 in ccRCC cells. Furthermore, we measured the migration and invasion abilities by using wound healing and transwell assays after overexpression or knockdown of TNFAIP8 in cells. In addition, we verified whether TNFAIP8 affects the EMT process in ccRCC by quantitative real-time PCR, western blotting, immunohistochemistry and immunofluorescence experiments. Results: Through database analysis, we found that TNFAIP8 was highly expressed in ccRCC patients and was positively correlated with tumor stage and grade, indicating that TNFAIP8 is associated with the development of advanced ccRCC and poor prognosis. We subsequently confirmed that TNFAIP8 was abnormally overexpressed in clinical samples and ccRCC cell lines and that TNFAIP8 promoted ccRCC cell migration and invasion in vitro. Finally, we found that TNFAIP8 regulated EMT-related molecule expression and regulated the EMT process. Conclusion: High expression of TNFAIP8 reinforces migration and regulates the EMT in ccRCC, conferring the metastatic potential of ccRCC and suggesting that TNFAIP8 may be a potential therapeutic target for the treatment of advanced ccRCC.

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Section: Discussionmentioning

confidence: 99%

TNFAIP8 promotes the migration of clear cell renal cell carcinoma by regulating the EMT

Zhong¹,

Zhu²,

Liu³

et al. 2020

J. Cancer

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“…Furthermore, several investigations have shown the great number of altered miRNA involved in renal cell carcinoma also [228,231,232,233,234,235,236,237,238,239,240,241,242,243,244,245,246,247,248]. These miRNA regulate cancer metastasis also, because of their capacity to inhibit numerous target genes involved in different steps of the metastatic cascade, e.g., EMT [233,241,244,245], migration [234,236,238,240,241,246], and metastasis settlement [231,235,239,242,243]. The variable interactions of all these miRNS in various tumor cells brings about manifold different capabilities for metastasis, which increases the odds that one of the embolized tumor cell exactly “fits” the properties of the target organ (soil)—a necessary prerequisite for the metastatic process.…”

Section: Discussionmentioning

confidence: 99%

Observations on Solitary Versus Multiple Isolated Pancreatic Metastases of Renal Cell Carcinoma: Another Indication of a Seed and Soil Mechanism?

Sellner¹

2019

Cancers

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Isolated pancreas metastases are a rare type of metastasis of renal cell carcinoma, characterized by the presence of pancreatic metastases, while all other organs remain unaffected. In a previous study, we determined arguments from the literature which (a) indicate a systemic–haematogenic metastasis route (uniform distribution of the metastases across the pancreas and independence of the metastatic localization in the pancreas of the side of the renal carcinoma); and (b) postulate a high impact of a seed and soil mechanism (SSM) on isolated pancreatic metastasis of renal cell carcinoma (isPM) as an explanation for exclusive pancreatic metastases, despite a systemic haematogenous tumor cell embolization. The objective of the study presented was to search for further arguments in favor of an SSM with isPM. For that purpose, the factor’s histology, grading, and singular/multiple pancreas metastases were analyzed on the basis of 814 observations published up to 2018. While histology and grading allowed for no conclusions regarding the importance of an SSM, the comparison of singular/multiple pancreas metastases produced arguments in favor of an SSM: 1. The multiple pancreas metastases observed in 38.1% prove that multiple tumor cell embolisms occur with isPM, the exclusive “maturation” of which in the pancreas requires an SSM; 2. The survival rates (SVR), which are consistent with singular and multiple pancreas metastases (despite the higher total tumor load with the latter), prove that the metastasized tumor cells are not able to survive in all other organs because of an SSM, which results in identical SVR when the pancreatic foci are treated adequately.

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“…The effect of an SSM brings about that those tumours will gain an advantage in metastasis settlement that produce a variety of cells with different metastatic potentials, as this increases the likelihood that a suitable tumour cell reaches a suitable host organ [ 20 ]. RCC is characterised by a high heterogeneity [ 140 , 155 , 160 ], for which a multitude of microRNA is co-responsible [ 161 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 , 172 , 173 , 174 ]. MicroRNAs control the metastasis capability through their ability to inhibit target genes involved in early steps of the metastatic cascade, e.g., epithelial–mesenchymal transition, migration, and metastasis settlement.…”

Section: Pathomechanisms Leading To Ispmrccmentioning

confidence: 99%

Tumour Evolution and Seed and Soil Mechanism in Pancreatic Metastases of Renal Cell Carcinoma

Sellner

Thalhammer

Klimpfinger

2021

Cancers

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In metastatic renal cell carcinoma, pancreatic metastases can appear in two clinical manifestations: (a) very rarely as isolated pancreatic metastases and (b) in the context with multi-organ metastatic disease. Both courses are characterised by rare, unusual clinical features. For isolated pancreatic metastases, the literature shows no effect on survival in all 11 publications that examined the effect of singular versus multiple pancreatic metastases; a lack of effect on survival time was also present in all 8 studies on pancreatic metastases size, in 7 of 8 studies on the influence of disease-free interval (DFI), and in 6 of 7 studies on the influence of synchronous versus metachronous metastases. In multi-organ site metastases observations, on the other hand, all five available references showed significantly better results in patients with concurrent pancreatic metastases compared to those without pancreatic metastases, although the total number of affected organs in the pancreatic metastases cohort was larger. Tumour volume-dependent risk factors thus remain surprisingly ineffective in both groups, which contradicts the usual behaviour of solid tumours. The reasons for this unusual behaviour and possible relations to tumour evolution and the hypothesis of an influence of a seed and soil mechanism in the occurrence of pancreatic metastases in metastatic renal cell carcinoma are discussed.

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MicroRNA‑218 inhibits the cell proliferation and migration in clear cell renal cell carcinoma through targeting cancerous inhibitor of protein phosphatase 2A

Cited by 10 publications

References 22 publications

TNFAIP8 promotes the migration of clear cell renal cell carcinoma by regulating the EMT

TNFAIP8 promotes the migration of clear cell renal cell carcinoma by regulating the EMT

Observations on Solitary Versus Multiple Isolated Pancreatic Metastases of Renal Cell Carcinoma: Another Indication of a Seed and Soil Mechanism?

Tumour Evolution and Seed and Soil Mechanism in Pancreatic Metastases of Renal Cell Carcinoma

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