MiR-106a-5p inhibits the cell migration and invasion of renal cell carcinoma through targeting PAK5

Pan, Yao‐Jie; Wei, Lulu; Wu, Xiaojin; Huo, Fu‐Chun; Mou, Jie; Pei, Dong‐Sheng

doi:10.1038/cddis.2017.561

Cited by 93 publications

(86 citation statements)

References 46 publications

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“…MiR‐28‐5p suppressed cell proliferation and migration by directly inhibiting RAP1B . MiR‐720 was significantly upregulated and had a clinical significance in RCC . The level of miR‐193a‐3p was evaluated in RCC patient serum .…”

Section: Discussionmentioning

confidence: 99%

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MiR‐193a‐3p and miR‐224 mediate renal cell carcinoma progression by targeting alpha‐2,3‐sialyltransferase IV and the phosphatidylinositol 3 kinase/Akt pathway

Pan

et al. 2018

Molecular Carcinogenesis

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Tumor metastasis is a major cause of cancer-related death in renal cell carcinoma (RCC). MicroRNAs (miRNAs) have been widely known to modulate proliferation invasion, metastasis, and apoptosis of cancer cells. In this study, we aimed to investigate the function and novel target of miR-193a-3p and miR-224 in RCC. The levels of miR-193a-3p and miR-224 were significantly increased in RCC tissues and RCC cell lines. Alpha-2,3-Sialyltransferase IV (ST3GalIV) was highly expressed in adjacent nontumor tissues and human normal proximal tubular cell line HK-2 compared to RCC tissues and cell lines. ST3GalIV expression was negatively correlated with miR-193a-3p and miR-224. Further analysis indicated that miR-193a-3p and miR-224 directly targeted ST3GalIV. MiR-193a-3p and miR-224 increased cell proliferation and migration by directly inhibiting ST3GalIV, and this effect was reversed by co-transfection with ST3GalIV in vitro. Overexpression of miR-193a-3p and miR-224 increased RCC cell proliferation in vivo. Furthermore, the phosphatidylinositol 3 kinase (PI3K)/Akt pathway was mediated by miR-193a-3p and miR-224 in RCC cell lines. Collectively, these results suggested that miR-193a-3p and miR-224 played an important role in regulation of RCC by targeting ST3GalIV via PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

“…23 MiR-720 was significantly upregulated and had a clinical significance in RCC. 25 The level of miR-193a-3p was evaluated in RCC patient serum. 16 However, the report about miR-193a-3p expression in RCC tissue and cell line was poor.…”

Section: Discussionmentioning

confidence: 99%

MiR‐193a‐3p and miR‐224 mediate renal cell carcinoma progression by targeting alpha‐2,3‐sialyltransferase IV and the phosphatidylinositol 3 kinase/Akt pathway

Pan

et al. 2018

Molecular Carcinogenesis

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“…Accumulating evidence has demonstrated that miRNAs are key gene regulators and are abnormally expressed in ccRCC (20,44,45). The dysregulation of miRNAs has been demonstrated to affect the initiation and progression of ccRCC (46,47).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑663 inhibits the proliferation and invasion of clear cell renal cell carcinoma cells by directly targeting PAK4

2018

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Accumulating evidence has demonstrated that microRNAs (miRNAs) are key gene regulators and are abnormally expressed in clear cell renal cell carcinoma (ccRCC). The dysregulation of miRNAs has been implicated in the initiation and progression of ccRCC. Therefore, identification of ccRCC-associated miRNAs may facilitate the determination of promising therapeutic targets for anti-cancer treatment.In the present study, miRNA-663 (miR-663) expression was downregulated in ccRCC tissues and cell lines. Functional experiments suggested that restoration of miR-663 expression inhibited the proliferation and invasion of ccRCC cells. In addition, p21 activated kinase 4 (PAK4) was validated as a direct target of miR-663 in ccRCC cells. PAK4 was upregulated in ccRCC tissues, and the expression level of PAK4 was inversely correlated with the miR-663 expression level. PAK4 restoration partially attenuated the suppressive roles of miR-663 overexpression on the proliferation and invasion of ccRCC cells. The present results provide novel insight into the mechanism underlying the occurrence and development of ccRCC, suggesting that the miR-663/PAK4 axis may be a novel therapeutic target for treatment of patients with ccRCC.

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“…Studies indicate that p21‐activated kinase 5 (PAK5), the most recently identified member of the PAK family, plays an indispensable role in regulation of the cytoskeleton, microtubule stability and cell survival . Increasing lines of evidence suggest that PAK5 is an oncogenic protein that is commonly overexpressed in many cancer tissues and contributes to the progression of diverse cancers . Likewise, in human breast cancer, PAK5 has been shown to activate a PAK5–early growth response protein 1 (Egr1)–matrix metalloproteinase 2 (MMP2) pathway to control cell migration and invasion .…”

Section: Introductionmentioning

confidence: 99%

“…5,6 Increasing lines of evidence suggest that PAK5 is an oncogenic protein that is commonly overexpressed in many cancer tissues and contributes to the progression of diverse cancers. [7][8][9][10][11] Likewise, in human breast cancer, PAK5 has been shown to activate a PAK5-early growth response protein 1 (Egr1)-matrix metalloproteinase 2 (MMP2) pathway to control cell migration and invasion. 12 PAK5-directed GATA1 phosphorylation has been reported to induce epithelialmesenchymal transition in breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

A PAK5–DNPEP–USP4 axis dictates breast cancer growth and metastasis

Geng

Zhang

et al. 2019

Intl Journal of Cancer

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Although clinically associated with the progression of multiple cancers, the biological function of p21‐activated kinase 5 (PAK5) in breast cancer remains largely unknown. Here, we reveal that the PAK5–aspartyl aminopeptidase (DNPEP)–ubiquitin‐specific protease 4 (USP4) axis is involved in breast cancer progression. We show that PAK5 interacts with and phosphorylates DNPEP at serine 119. Functionally, we demonstrate that DNPEP overexpression suppresses breast cancer cell proliferation and invasion and restricts breast cancer growth and metastasis in mice. Furthermore, we identify USP4 as a downstream target of the PAK5–DNPEP pathway; DNPEP mediates USP4 downregulation. Importantly, we verify that DNPEP expression is frequently downregulated in breast cancer tissues and is negatively correlated with PAK5 and USP4 expression. PAK5 decreases DNPEP abundance via the ubiquitin–proteasome pathway. Consistently, analyses of clinical breast cancer specimens revealed significantly increased PAK5 and USP4 levels and an association between higher PAK5 and USP4 expression and worse breast cancer patient survival. These findings suggest a pivotal role for PAK5‐elicited signaling in breast cancer progression.

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MiR-106a-5p inhibits the cell migration and invasion of renal cell carcinoma through targeting PAK5

Cited by 93 publications

References 46 publications

MiR‐193a‐3p and miR‐224 mediate renal cell carcinoma progression by targeting alpha‐2,3‐sialyltransferase IV and the phosphatidylinositol 3 kinase/Akt pathway

MiR‐193a‐3p and miR‐224 mediate renal cell carcinoma progression by targeting alpha‐2,3‐sialyltransferase IV and the phosphatidylinositol 3 kinase/Akt pathway

MicroRNA‑663 inhibits the proliferation and invasion of clear cell renal cell carcinoma cells by directly targeting PAK4

A PAK5–DNPEP–USP4 axis dictates breast cancer growth and metastasis

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