MiR-200c-3p inhibits cell migration and invasion of clear cell renal cell carcinoma via regulating SLC6A1

Maolakuerban, Naibijiang; Azhati, Baihetiya; Tusong, Hamulati; Abula, Asimujiang; Yasheng, Anniwaer; Xireyazidan, Ayiding

doi:10.1080/15384047.2017.1394551

Cited by 37 publications

(31 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Using the miRNA target prediction algorithm TargetScan (http://www.targetscan.org), we determined that HMGB3 was a predicted target of miR‐200b‐3p and miR‐200c‐3p (Figure A). Crucially, both miR‐200b‐3p and miR‐200c‐3p have been shown to act as tumour suppressors during cancer development . In order to confirm the TargetScan prediction, we performed luciferase assays by cotransfecting miR‐200b‐3p and miR‐200c‐3p with wild‐type or mutated 3′‐UTR of HMGB3 into HEK293 cells (Figure B).…”

Section: Resultsmentioning

confidence: 99%

“…Crucially, both miR-200b-3p and miR-200c-3p have been shown to act as tumour suppressors during cancer development. 27,28 In order to confirm the TargetScan prediction, we performed luciferase assays by cotransfecting miR-200b-3p and miR-200c-3p with wild-type or mutated 3′-UTR of HMGB3 into HEK293 cells ( Figure 5B). Luciferase activity driven by the 3′-UTR of HMGB3 was significantly decreased in the presence of miR-200b-3p and miR-200c-3p ( Figure 5C).…”

Section: Hmgb3 Is Targeted By Mir-200b-3p and Mir-200c-3pmentioning

confidence: 99%

See 1 more Smart Citation

HMGB3 promotes the proliferation and metastasis of glioblastoma and is negatively regulated by miR‐200b‐3p and miR‐200c‐3p

Liu

Wang

2018

Cell Biochemistry & Function

View full text Add to dashboard Cite

High mobility group box 3 (HMGB3) is strongly involved in oncogenesis in a variety of cancers. In the present study, we have explored the role of HMGB3 in glioblastoma multiforme (GBM) tumorigenesis and have identified the microRNAs (miRNAs) miR-200b-3p and miR-200c-3p as negative regulators of HMGB3 expression. We began by determining that endogenous HMGB3 expression levels were significantly elevated in GBM tissues and in 3 GBM cell lines. To study the function of HMGB3 in GBM, we transfected a small-interfering RNA (siRNA) against HMGB3 into GBM cell lines U251 and LN229. MTT and tumour sphere assays demonstrated that HMGB3 knockdown significantly inhibited cell proliferation. Wound healing and transwell assays determined that HMGB3 knockdown substantially suppressed GBM cell migration and invasion. We evaluated the effects of HMGB3 knockdown on MAPK phosphorylation and target gene expression, finding that HMGB3 knockdown significantly reduced MAPK phosphorylation (p-ERK (1/2), p-p38, and p-JNK). We then used the biologic prediction algorithm TargetScan to identify the 3' untranslated region (3'-UTR) of HMGB3 as a target of miR-200b-3p and miR-200c-3p. Luciferase, qRT-PCR, and western blot assays confirmed that miR-200b-3p and miR-200c-3p bind and inhibit HMGB3 expression. Finally, Pearson correlation analyses demonstrated a negative correlation between relative HMGB3 mRNA and miR-200b/c-3p expression levels in GBM tissue samples. Overall, the present study strongly suggests that HMGB3 promotes GBM oncogenesis through the MAPK signalling pathway while miR-200b-3p and miR-200c-3p inhibit its expression.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Hmgb3 Is Targeted By Mir-200b-3p and Mir-200c-3pmentioning

confidence: 99%

HMGB3 promotes the proliferation and metastasis of glioblastoma and is negatively regulated by miR‐200b‐3p and miR‐200c‐3p

Liu

Wang

2018

Cell Biochemistry & Function

View full text Add to dashboard Cite

show abstract

“…miRNAs are known to be an integral component of cancer development [17][18][19]. Several studies have highlighted the role of miR-182-5p in the development of different cancers [13,14].…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning

confidence: 99%

miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1

Nan

Zhong

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of miR-182-5p in OSCC by targeting the calcium/ calmodulin-dependent protein kinase II inhibitor CAMK2N1. Methods: miR-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed. Results: miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-κB. Mice injected with CAL-27 cells transfected with miR-182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group. Conclusion: The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells.

show abstract

“…MiRNAs have essential biological roles and clinical implication in CCRCC [33]. MiR-200c-3p was shown to restrain CCRCC cell migration and invasion by targeting Solute Carrier Family 6 Member 1 (SLC6A1) [34], and miR-122 acted as a tumor promoter of CCRCC via down-regulating Forked-box class O3 (FOXO3) [35]. Herein, we found that miR-1233 directly targeted ACAT2 to be a pro-cancer molecule of CCRCC.…”

Section: Discussionmentioning

confidence: 94%

Circ_RPL23A acts as a miR-1233 sponge to suppress the progression of clear cell renal cell carcinoma by promoting ACAT2

Cheng

Cao

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Clear cell renal cell carcinoma (CCRCC) is a prevalent urological carcinoma with high metastatic risk. Circular RNAs (circRNAs) have been identified as effective diagnostic and therapeutic biomarkers for CCRCC. This research aims to disclose the involvement of circRNA ribosomal protein L23a (circ_RPL23A) in CCRCC, and how it regulates carcinogenesis. Methods We performed quantitative real-time polymerase chain reaction (qRT-PCR) to examine circ_RPL23A, microRNA-1233 (miR-1233) and acetyl-coenzyme A acetyltransferase 2 (ACAT2). Cellular behavior detection included cell cycle, proliferation, apoptosis and metastasis, which were severally analyzed using propidium iodide (PI)-flow cytometry, 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), Annexin V/PI-flow cytometry and transwell migration/invasion assays. ACAT2 and related proteins of cell cycle, epithelial-mesenchymal transition (EMT) were measured via western blot. Target relationship was analyzed via dual-luciferase reporter assay. A xenograft model was used to study circ_RPL23A action in mice. Results Both in CCRCC tissues and cells, circ_RPL23A had a down-regulated tendency. Explicitly, circ_RPL23A overexpression inhibited cell cycle, proliferation and metastasis but enhanced apoptosis of CCRCC cells, whereas these effects of circ_RPL23A were dependent on the suppression of its target miR-1233. Besides, miR-1233 could target ACAT2 and circ_RPL23A regulated ACAT2 by sponging miR-1233. Also importantly, miR-1233 was a pro-cancer gene in CCRCC via targeting ACAT2. CCRCC tumor growth was also decreased in vivo by circ_RPL23A through miR-1233/ACAT2 axis. Conclusion Altogether, the circ_RPL23A/miR-1233/ACAT2 axis in this report provides an in-depth cognition for CCRCC pathogenesis and circ_RPL23A may has pivotal value in diagnosing and treating CCRCC.

show abstract

MiR-200c-3p inhibits cell migration and invasion of clear cell renal cell carcinoma via regulating SLC6A1

Cited by 37 publications

References 36 publications

HMGB3 promotes the proliferation and metastasis of glioblastoma and is negatively regulated by miR‐200b‐3p and miR‐200c‐3p

HMGB3 promotes the proliferation and metastasis of glioblastoma and is negatively regulated by miR‐200b‐3p and miR‐200c‐3p

miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1

Circ_RPL23A acts as a miR-1233 sponge to suppress the progression of clear cell renal cell carcinoma by promoting ACAT2

Contact Info

Product

Resources

About