Evidence map›Paper›PMID 32550826›Full record

ArticleCancer cell international2020

CircHIPK3 promotes proliferation and metastasis and inhibits apoptosis of renal cancer cells by inhibiting MiR-485-3p.

Jinjin Lai, Jun Xin, Changde Fu, Wei Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.

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  7. [Research Progress of Circular RNA CircHIPK3 in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024
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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

4 authors at 1 institution in 1 country.

Jinjin LaiDepartment of Urology, Quanzhou First Hospital Affiliated to Fujian Medical University, 248-252 East Street, Licheng District, Quanzhou, 362002 Fujian Province China.ORCID 0000-0002-3109-5079
Jun XinDepartment of Urology, Quanzhou First Hospital Affiliated to Fujian Medical University, 248-252 East Street, Licheng District, Quanzhou, 362002 Fujian Province China.
Changde FuDepartment of Urology, Quanzhou First Hospital Affiliated to Fujian Medical University, 248-252 East Street, Licheng District, Quanzhou, 362002 Fujian Province China.
Wei ZhangDepartment of Urology, Quanzhou First Hospital Affiliated to Fujian Medical University, 248-252 East Street, Licheng District, Quanzhou, 362002 Fujian Province China.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe intervention of circHIPK3 in renal carcinoma (RC) has not been reported, and thus, the current study investigated the intervention and mechanism of circHIPK3 in RC.

methodsThe expression of circHIPK3 in RC tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Ribonuclease R (RNase R) resistance and distribution of circHIPK3 and HIPK3 were analyzed by RNase R digestion experiments and cytoplasm/nucleus separation experiments. CircHIPK3 was knocked down in ACHN and 769-P cells. Cell counting kit-8 (CCK-8), colony formation assay, scratch assay, and Transwell assay were performed to detect cell proliferation and metastasis. CircInteractome, qRT-PCR and dual-luciferase reporter assay were used to predict the target miRNAs of circHIPK3. Furthermore, a series of rescue experiments were performed to analyze the regulatory relationship between circHIPK3 and miR-485-3p. Epithelial-mesenchymal transition (EMT) and the expressions of apoptosis-associated markers were detected by Western blot and qRT-PCR. The regulatory relationship between circHIPK3 and miR-485-3p in vivo was explored by xenograft experiments, Western blot, qRT-PCR and immunohistochemistry (Ki-67).

resultsCircHIPK3 was mainly overexpressed in the cytoplasm of RC tissues and cells. Knocking down circHIPK3 inhibited the proliferation, migration, and invasion of RC cells. The expression of circHIPK3 was negatively related to that of its target gene miR-485-3p. Results of the rescue experiments showed that circHIPK3 overexpression could partially reverse the anti-carcinoma effect of miR-485-3p mimic. The specific mechanism of circHIPK3 was related to the effect of miR-485-3p on partially reversing the up-regulated expressions of Clever caspase-3, Bax, E-Cadherin and down-regulated expressions of Bcl-2, N-Cadherin and Vimentin. The results of in vivo experiments demonstrated that circHIPK3 promoted tumor growth and the expression of Ki-67 by down-regulating miR-485-3p.

conclusionCircHIPK3 promotes the proliferation and metastasis and inhibits the apoptosis of RC cells through competitively binding to miR-485-3p.

Indexed as

ApoptosiscircHIPK3Epithelial-mesenchymal transitionmiR-485-3pRenal carcinoma

Identifiers

PMID32550826
PMCPMC7298839
OpenAlexW3034792907

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.