Evidence mapPaperPMID 30745845Full record

ArticleInternational journal of biological sciences2019

TRIB3 Promotes the Proliferation and Invasion of Renal Cell Carcinoma Cells via Activating MAPK Signaling Pathway.

Baoan Hong, Jingcheng Zhou, Kaifang Ma, Jiufeng Zhang, Haibiao Xie, Kenan Zhang, Lei Li, Lin Cai, Ning Zhang, Zhongyuan Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 95 citations in OpenAlex.

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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 2 institutions in 1 country.

Baoan HongDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Jingcheng ZhouDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Kaifang MaDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Jiufeng ZhangDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Haibiao XieDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Kenan ZhangDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Lei LiDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Lin CaiDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Ning ZhangDepartment of Urology, Beijing Cancer Hospital, Beijing 100142, P.R. China.
Zhongyuan ZhangDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Kan GongDepartment of Urology, Peking University First Hospital, Beijing 100034, P.R. China.
Peking University First Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tribbles pseudokinase 3 (TRIB3) is a member of the mammalian pseudokinase tribbles family and is involved in multiple biological processes. However, the role of TRIB3 in renal cell carcinoma (RCC) remains unclear. In this study, we aimed to elucidate the biological functions of TRIB3 in RCC and explore its underlying mechanisms. TRIB3 expression and its correlation with clinicopathological features was evaluated in 123 patients with RCC. A series of cytological experiments were performed to clarify the biological functions of TRIB3, and potential molecular regulatory mechanisms were explored using transcriptome sequencing. TRIB3 expression was significantly elevated in RCC tissues compared to that in paracancerous tissues, and high expression of TRIB3 was correlated with both advanced tumor stage and unfavorable prognosis. TRIB3 knockdown markedly inhibited RCC cell proliferation, migration and invasion. Furthermore, overexpression of TRIB3 promoted RCC cell proliferation, migration, invasion and xenograft tumor growth. Notably, TRIB3 expression was modulated by hypoxia-inducible factor-1α (HIF-1α), which enhanced cell viability and invasiveness via targeting the MAPK signaling pathway. This study reveals the potential oncogenic role of TRIB3 in RCC pathogenesis and illustrates the mechanisms underlying TRIB3-mediated tumor progression, providing new insight into the development of TRIB3 as a tumor biomarker and therapeutic target.

Indexed as

AnimalsBlotting, WesternCarcinoma, Renal CellCell Cycle ProteinsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Signaling SystemMice, Inbred BALB CProtein Serine-Threonine KinasesRepressor ProteinsSignal TransductionWound HealingCell Cycle ProteinsProtein Serine-Threonine KinasesRepressor ProteinsTRB3 protein, mouseTRIB3 protein, humancell invasioncell proliferationmitogen-activated protein kinasesrenal cell carcinomaTribbles pseudokinase 3

Identifiers

PMID30745845
PMCPMC6367588
OpenAlexW2910514691

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.