Micro<scp>RNA</scp>‐301b‐3p contributes to tumour growth of human hepatocellular carcinoma by repressing vestigial like family member 4

Guo, Yang; Yao, Bowen; Zhu, Qiaojuan; Xiao, Zunqiang; Hu, Linjun; Liu, Xin; Li, Lijie; Wang, Jiahui; Xu, Qiuran; Liu, Yang; Huang, Dongsheng

doi:10.1111/jcmm.14361

Cited by 29 publications

(20 citation statements)

References 35 publications

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“…An in vivo tumor growth assay was performed using BALB/C nude mice as previously described 18 . Briefly, 1 × 10 6 Hep3B cell with or without LINC01123 knockdown were injected subcutaneously into nude mice (n=5 per group).…”

Section: Methodsmentioning

confidence: 99%

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Xiao¹,

Liu

Zhao³

et al. 2020

Int. J. Biol. Sci.

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Hepatocellular carcinoma (HCC), one of the main causes of cancer-related deaths globally, is characterized by rapid growth and high invasiveness. Accumulating evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in the growth and metastasis of HCC. Recently, lncRNA LINC01123 has been found to contribute to cell proliferation and aerobic glycolysis in lung cancer. However, the function of LINC01123 in HCC, as well as the underlying mechanism of its action, remain unclear. Here, we found that the expression of LINC01123 was clearly upregulated in HCC tissues compared to nontumor tissues. Furthermore, expression of LINC01123 in HCC cells was significantly higher than in LO2 cells. Importantly, the upregulated level of LINC01123 was related to unfavorable clinical features and poor prognosis of HCC. Next, we demonstrated that LINC01123 knockdown suppressed the proliferation, migration and invasion of HCC cells in vitro . Depletion of LINC01123 inhibited HCC xenograft growth in vivo . Conversely, ectopic expression of LINC01123 facilitated HCC cell proliferation and invasion. Mechanistically, LINC01123 acted as a molecular sponge for miR-34a-5p in HCC cells. Tuftelin1 (TUFT1) was identified as the target gene of miR-34a-5p. LINC01123 positively regulated TUFT1 level by targeting of miR-34a-5p in HCC cells. Notably, TUFT1 restoration can abolish miR-34a-5p-induced inhibitory effects on HCC cell proliferation, migration and invasion. In conclusion, LINC01123 was overexpressed in HCC and accelerated cancer cell proliferation and invasion by regulating the miR-34a-5p/TUFT1 axis.

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Section: Methodsmentioning

confidence: 99%

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Xiao¹,

Liu

Zhao³

et al. 2020

Int. J. Biol. Sci.

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“…Four-week BALB/c nude mice were purchased from Shanghai SLAC Laboratory Animal Company (Shanghai, China). The in vivo tumor growth and lung metastasis experiments were performed using Hep3B cells with or without USP13 knockdown according to the protocols as previously described (Dou et al, 2019a;Guo et al, 2019). The tumor volume (V) was calculated as follows: V = (L × D2)/2 where L and D represent the tumor length and width, respectively (in mm).…”

Section: In Vivo Experimentsmentioning

confidence: 99%

Hypoxia-Inducible Ubiquitin Specific Peptidase 13 Contributes to Tumor Growth and Metastasis via Enhancing the Toll-Like Receptor 4/Myeloid Differentiation Primary Response Gene 88/Nuclear Factor-κB Pathway in Hepatocellular Carcinoma

Gao

Chen

et al. 2020

Front. Cell Dev. Biol.

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“…Survival analysis indicated that the survival time of patients with high miR-301b-3p expression was markedly shorter than that of patients with low miR-301b-3p expression; hence, miR-301b-3p was likely to be the disadvantageous prognostic factor of breast cancer ( Figure 1(b) ). Besides, miR-301b-3p is considered to be an oncogene in many researches [ 15 , 16 ]. Accordingly, we detected its expression in breast cancer cells ( Figure 1(c) ) and found that its expression in breast cancer cells MCF7, MDA-MB-231, and SK-BR-3 was noticeably higher than that in normal breast cell Hs 578Bst.…”

Section: Resultsmentioning

confidence: 99%

miR-301b-3p Regulates Breast Cancer Cell Proliferation, Migration, and Invasion by Targeting NR3C2

Fan

Zhu

et al. 2021

Journal of Oncology

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Objectives. Breast cancer is the most common malignant tumor among females, and miRNAs have been reported to play an important regulatory role in breast cancer progression. This study aimed to explore the function and underlying molecular mechanism of miR-301b-3p in breast cancer. Methods. Differential analysis and survival analysis were performed based on the data accessed from the TCGA-BRCA dataset for identification of the target miRNA. Bioinformatics analysis was conducted to predict the downstream target gene of the miRNA. Real-time quantitative PCR was carried out to detect the expression of miR-301b-3p and nuclear receptor subfamily 3 group C member 2 (NR3C2). Western blot was used to assess the protein expression of NR3C2. Cell counting kit-8 assay was performed to evaluate the proliferation of breast cancer cells. Transwell assay was conducted to determine the migratory and invasive abilities of breast cancer cells. Dual-luciferase reporter assay was employed to verify the targeting relationship between miR-301b-3p and NR3C2. Results. miR-301b-3p was elevated in breast cancer cell lines and promoted cell proliferation, migration, and invasion in terms of its biological function in breast cancer. NR3C2 was validated as a direct target of miR-301b-3p via bioinformatics analysis and dual-luciferase reporter assay, and NR3C2 was downregulated in breast cancer cell lines. The rescue experiment indicated that NR3C2 was involved in the mechanism by which miR-301b-3p regulated the malignant phenotype of breast cancer cells. Conclusion. The present study revealed for the first time that miR-301b-3p could foster breast cancer cell proliferation, migration, and invasion by targeting NR3C2, unveiling that miR-301b-3p is a novel carcinogen in breast cancer.

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MicroRNA‐301b‐3p contributes to tumour growth of human hepatocellular carcinoma by repressing vestigial like family member 4

Cited by 29 publications

References 35 publications

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Hypoxia-Inducible Ubiquitin Specific Peptidase 13 Contributes to Tumor Growth and Metastasis via Enhancing the Toll-Like Receptor 4/Myeloid Differentiation Primary Response Gene 88/Nuclear Factor-κB Pathway in Hepatocellular Carcinoma

miR-301b-3p Regulates Breast Cancer Cell Proliferation, Migration, and Invasion by Targeting NR3C2

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