Downregulation of long non-coding RNA LINC00460 inhibits the proliferation, migration and invasion, and promotes apoptosis of pancreatic cancer cells via modulation of the miR-320b/ARF1 axis

Cheng, Jian; Lou, Yanghui; Jiang, Kai

doi:10.1080/21655979.2020.1863035

Cited by 28 publications

(21 citation statements)

References 28 publications

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“…After 48 h, the invaded cells were fixed with 4% paraformaldehyde, washed twice with PBS, and stained with 0.1% crystal violet. Subsequently, the invaded cells were imaged under a microscope (Olympus, Japan) [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

MicroRNA hsa-miR-150-5p inhibits nasopharyngeal carcinogenesis by suppressing PYCR1 (pyrroline-5-carboxylate reductase 1)

Zhou

Huang

et al. 2021

Bioengineered

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Nasopharyngeal cancer is a rare cancer type, but with a low five-year survival rate. Dysregulation of pyrroline-5-carboxylate reductase 1 (PYCR1) and microRNA hsa-miR-150-5p is involved in the development of various cancers. However, the molecular mechanism of the hsa-miR-150-5p-PYCR1 axis in nasopharyngeal cancer remains unclear. To identify the mechanism of the hsa-miR-150-5p-PYCR1 axis, the expression of hsa-miR-150-5p and PYCR1 in nasopharyngeal cancer tissues and cells was first measured by reverse transcription quantitative polymerase chain reaction. The luciferase and RNA pull-down assays were used to confirm the interaction between hsa-miR-150-5p and PYCR1. The overexpression of hsa-miR-150-5p and PYCR1 was detected by cell viability, proliferation, western blotting, migration, and invasion in nasopharyngeal cancer cells. The expression levels of hsa-miR-150-5p was reduced in the nasopharyngeal cancer tissues and cells and were negatively correlated with the PYCR1 levels. The upregulation of hsa-miR-150-5p significantly repressed cell growth and promoted apoptosis. However, the upregulation of PYCR1 expression significantly promoted nasopharyngeal carcinogenesis, which could abolish the inhibitory effect of hsa-miR-150-5p. In conclusion, we clarified that hsa-miR-150-5p attenuated nasopharyngeal carcinogenesis by reducing the PYCR1 expression levels. This provides a new perspective of nasopharyngeal cancer involving both hsa-miR-150-5p and PYCR1 for the treatment of nasopharyngeal cancer.

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Section: Methodsmentioning

confidence: 99%

MicroRNA hsa-miR-150-5p inhibits nasopharyngeal carcinogenesis by suppressing PYCR1 (pyrroline-5-carboxylate reductase 1)

Zhou

Huang

et al. 2021

Bioengineered

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“…Cell viability was assessed by using CCK-8 assays [ 15 ]. First, cells were seeded in 96-well plates at a density of 5,000 cells per well.…”

Section: Methodsmentioning

confidence: 99%

Apcin inhibits the growth and invasion of glioblastoma cells and improves glioma sensitivity to temozolomide

Ding

Zhang

et al. 2021

Bioengineered

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Glioblastoma (GBM) is the most common malignant primary brain tumor, and GBM patients have a poor overall prognosis. CDC20 expression is increased in a variety of tumors and associated with temozolomide (TMZ) resistance in glioma cells. Apcin specifically binds to CDC20 to inhibit APC/C-CDC20 interaction and exhibits antitumor properties. The purpose of this article was to assess whether apcin inhibits tumor growth in glioma cell lines and increases the sensitivity of GBM to TMZ. In this study, a series of biochemical assays, such as Cell Counting Kit-8 (CCK-8), wound healing, apoptosis and colony formation assays, were performed to determine the antitumor properties of apcin in glioma cells. GBM cell apoptosis was detected by western blotting analysis of related proteins. Apcin increased the sensitivity of glioma to TMZ, as confirmed by CCK-8 and western blotting analysis. The results showed that apcin significantly inhibited the proliferation of glioma cells in a time- and dose-dependent manner. The migration decreased with increasing apcin concentrations. Increased Bim expression indicated that apcin promotes the apoptosis of glioma cells. Furthermore, apcin improved glioma sensitivity to TMZ. The results showed that apcin can effectively inhibit GBM growth and improve TMZ sensitivity. Apcin has the potential to treat GBM and is expected to provide new ideas for individualized treatment.

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“…Anti-miR-1255b-5p or miR-1255b-5p transfected 22Rv1 and DU 145 cells were transfected with pmirGLO vectors. Then the luciferase activity was tested at 48 hours after transfection at a Dual-Luciferase Reporter Assay System (Promega, Australia) as per the manufacturer’s instructions [ 24 ]. The final data was shown as relative luciferase activity by firefly luciferase/Renilla luciferase.…”

Section: Methodsmentioning

confidence: 99%

Diagnostic significance of microRNA-1255b-5p in prostate cancer patients and its effect on cancer cell function

et al. 2021

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Discerning between indolent and aggressive types is a big challenge of prostate cancer clinically to guide the adequate therapeutic regimen. We aimed to examine the relationship between miR-1255b-p expression and prostate cancer and elucidate the function of miR-1255b-5p in prostate cancer. miR-1255b-5p were measured using Quantitative Real-Time PCR from the blood 103 benign prostate hyperplasia (BPH) and 153 prostate cancer patients (117 indolent cases and 36 upgrading cases). Using receiver operating characteristic (ROC) curve analysis, the discriminating ability of miR-1255b-5p was accessed between BPH and prostate cancer participants, or indolent and aggressive type. Using CCK-8 and Transwell assays, the function of miR-1255b-5p on prostate cancer cells was investigated. The levels of miR-1255b-5p were significantly raised in prostate cancer patients when compared with BPH participants. MiR-1255b-5p level can distinguish prostate cancer patients from BPH or indolent type from aggressive type. Downregulation of miR-1255b-5p can suppress the proliferative, invasive, and migratory capacity, but this effect can be eradicated by EPB41L1 inhibition. The measurement of miR-1255b-5p in blood may provide a new noninvasive approach for the diagnosis of prostate cancer. miR-1255b-5p may become a potential therapeutic target for prostate cancer.

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Downregulation of long non-coding RNA LINC00460 inhibits the proliferation, migration and invasion, and promotes apoptosis of pancreatic cancer cells via modulation of the miR-320b/ARF1 axis

Cited by 28 publications

References 28 publications

MicroRNA hsa-miR-150-5p inhibits nasopharyngeal carcinogenesis by suppressing PYCR1 (pyrroline-5-carboxylate reductase 1)

MicroRNA hsa-miR-150-5p inhibits nasopharyngeal carcinogenesis by suppressing PYCR1 (pyrroline-5-carboxylate reductase 1)

Apcin inhibits the growth and invasion of glioblastoma cells and improves glioma sensitivity to temozolomide

Diagnostic significance of microRNA-1255b-5p in prostate cancer patients and its effect on cancer cell function

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