Evidence map›Paper›PMID 33775245›Full record

ArticleBMC urology2021

Let-7i-5p enhances cell proliferation, migration and invasion of ccRCC by targeting HABP4.

Yujie Liu, Xing Hu, Liang Hu, Changjing Xu, Xuemei Liang

Open access · goldAbstract read
In one paragraph

Article in BMC urology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-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

16 citing papers in PubMed, 29 citations in OpenAlex.

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  8. Role of SYT11 in human pan-cancer using comprehensive approaches.European journal of medical research · 2024
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  10. LetZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
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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

5 authors at 1 institution in 1 country.

Yujie Liu *Department of Geriatric Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Xing Hu *Department of General Practice, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Liang HuDepartment of Cardiovascular Surgery, The General Hospital of Western Theater Command, Chengdu, 610083, China.
Changjing XuDepartment of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Xuemei LiangDepartment of Geriatric Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. xuemei_liang@163.com.
Affiliated Hospital of Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClear cell renal cell carcinoma (ccRCC) is one of the best-characterized and most pervasive renal cancers. The present study aimed to explore the effects and potential mechanisms of let-7i-5p in ccRCC cells.

methodsUsing bioinformatics analyses, we investigated the expression of let-7i-5p in The Cancer Genome Atlas (TCGA) database and predicted biological functions and possible target genes of let-7i-5p in ccRCC cells. Cell proliferation assay, wound healing assay and transwell invasion assay were conducted to characterize the effects of let-7i-5p in ccRCC cells. To verify the interactions between let-7i-5p and HABP4, dual-luciferase reporter assay, quantitative real-time polymerase chain reaction, and western blotting were conducted. Rescue experiments were used to investigate the relationship between let-7i-5p and HABP4.

resultsTCGA data analysis revealed that ccRCC tissues had significantly increased let-7i-5p expression, which was robustly associated with poor overall survival. Further verification showed that ccRCC cell proliferation, migration and invasion were inhibited by let-7i-5p inhibitor but enhanced by let-7i-5p mimics. Subsequently, HABP4 was predicted to be the target gene of let-7i-5p. TCGA data showed that ccRCC tissues had decreased expression of HABP4 and that HABP4 expression was negatively correlated with let-7i-5p. Further verification showed that downregulation of HABP4 expression promoted cell proliferation, migration and invasion. The dual-luciferase reporter gene assay suggested that the let-7i-5p/HABP4 axis was responsible for the development of ccRCC.

conclusionOur results provide evidence that let-7i-5p functions as a tumor promoter in ccRCC and facilitates cell proliferation, migration and invasion by targeting HABP4. These results clarify the pathogenesis of ccRCC and offer a potential target for its treatment.

Indexed as

Carcinoma, Renal CellCell MovementCell ProliferationFemaleHumansKidney NeoplasmsMaleMicroRNAsMiddle AgedMyogenic Regulatory FactorsNeoplasm InvasivenessTumor Cells, CulturedHABP4 protein, humanMicroRNAsmirnlet7 microRNA, humanMyogenic Regulatory FactorsCell invasionCell migrationCell proliferationClear cell renal cell carcinomaHABP4Let-7i-5p

Identifiers

PMID33775245
PMCPMC8005230
OpenAlexW3149338389

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.