ArticleRSC advances2019
Retracted Article: MicroRNA-1271 modulates hepatitis B virus replication, cell proliferation and apoptosis in hepatitis B virus-related hepatocellular carcinoma by targeting SIRT1.
Article in RSC advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 0 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B virus (HBV) infection is a leading cause of hepatocellular carcinoma (HCC). Certain studies have revealed that microRNAs play crucial roles in HBV-related HCC. The aim of this study was to investigate the effects of microRNA-1271 (miR-1271) on HBV replication, cell proliferation and apoptosis in HBV-related HCC. The expression of HBV DNA and miR-1271 was detected by quantitative real time-polymerase chain reaction (qRT-PCR). The mRNA and protein levels of SIRT1 were detected by qRT-PCR and western blot analysis, respectively. HBV replication was assessed by the expression of HBV DNA and the levels of HBsAg and HBeAg. Cell proliferation was assessed by cell counting kit-8 (CCK-8) and 5-bromo-2-deoxyuidine (BrdU) assay, and apoptosis was evaluated by flow cytometry assay, enzyme-linked immunosorbent assay (ELISA) and the activity of caspase-3. The relationship between miR-1271 and SIRT1 was predicated by online software and confirmed by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) and pull-down assay. We first found that the expression of miR-1271 was downregulated and SIRT1 was upregulated in both HBV-related HCC tissues and cells. Overexpression of miR-1271 inhibited HBV replication and cell proliferation whilst promoting apoptosis in HBV-related HCC cells. Subsequently, SIRT1 was identified as a target of miR-1271. Moreover, overexpression of SIRT1 reversed the effects of miR-1271 overexpression on HBV replication, cell proliferation and apoptosis in HBV-related HCC cells. In conclusion, our study demonstrated that miR-1271 inhibited HBV replication and proliferation and promoted apoptosis of HBV-related HCC cells
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.