Evidence map›Paper›PMID 27062697›Full record

ArticleCancer biomarkers : section A of Disease markers2016

Mir-765 promotes cell proliferation by downregulating INPP4B expression in human hepatocellular carcinoma.

Bin-Hui Xie, Xiao He, Rui-Xi Hua, Bing Zhang, Guo-Sheng Tan, Shi-Qiu Xiong, Liang-Shuai Liu, Wei Chen, Jian-Yong Yang, Xiao-Nong Wang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer biomarkers : section A of Disease markers, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Microrna Expression inMicroRNA (Shariqah, United Arab Emirates) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Bin-Hui XieDepartment of General Surgery, the First Affiliated Hospital of Gannan Medical University, Guangzhou, Guangdong, China.
Xiao HeDepartment of General Surgery, the First Affiliated Hospital of Gannan Medical University, Guangzhou, Guangdong, China.
Rui-Xi HuaDepartment of Oncology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Bing ZhangDepartment of Nuclear Medicine, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Guo-Sheng TanDepartment of Interventional Radiology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Shi-Qiu XiongDepartment of Biochemistry, University of Leicester, Leicester, UK.
Liang-Shuai LiuDepartment of Interventional Radiology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Wei ChenDepartment of Interventional Radiology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Jian-Yong YangDepartment of Interventional Radiology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Xiao-Nong WangDepartment of General Surgery, the First Affiliated Hospital of Gannan Medical University, Guangzhou, Guangdong, China.
He-Ping LiDepartment of Oncology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNFirst Affiliated Hospital of Gannan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNAs (miRNAs) dysregulation is widely involved in cancer progression and contributed to sustained cell proliferation by directly targeting multiple targets. Therefore, better understanding the underlying mechanism of miRNA in carcinogenesis may improve diagnostic and therapeutic strategies for malignancy. In our study, we found that mir-765 is upregulated in both hepatocellular carcinoma (HCC) cell lines and tissues, compared to human normal liver cell line and adjacent non-cancerous tissues, respectively. Overexpression of mir-765 increased HCC cells proliferation and tumorigenicity, whereas inhibition of mir-765 reverses this effect. Furthermore, we demonstrated that INPP4B as a direct target of mir-765 and ectopic expression of mir-765 repressed INPP4B expression, resulting in upregulation of p-AKT, Cyclin D1, and downregulation of p-FOXO3a, p21 expression in HCC. Strikingly, we found that silencing the expression of INPP4B is the essential biological function of miR-765 during HCC cell proliferation. Collectively, our findings reveal that miR-765 is a potential onco-miR that participates in carcinogenesis of human HCC by suppressing INPP4B expression, and might represent a potential therapeutic target for HCC patients.

Indexed as

Carcinoma, HepatocellularCell Line, TumorCell ProliferationCell Transformation, NeoplasticCyclin D1Cyclin-Dependent Kinase Inhibitor p21Down-RegulationForkhead Box Protein O3Gene Expression Regulation, NeoplasticHumansLiver NeoplasmsMicroRNAsPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-aktCCND1 protein, humanCyclin D1Cyclin-Dependent Kinase Inhibitor p21Forkhead Box Protein O3FOXO3 protein, humanMicroRNAsMIRN765 microRNA, humanphosphatidylinositol-3,4-bisphosphate 4-phosphatasePhosphoric Monoester HydrolasesProto-Oncogene Proteins c-akthuman hepatocellular carcinomaINPP4BmiR-765proliferation

Identifiers

PMID27062697
PMCPMC13016493
OpenAlexW2296384492

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.