Evidence map›Paper›PMID 35847878›Full record

ArticleFrontiers in oncology2022

RAC3 Inhibition Induces Autophagy to Impair Metastasis in Bladder Cancer Cells

Liwei Wang, Jiazhong Shi, Sha Liu, Yaqin Huang, Hua Ding, Baixiong Zhao, Yuting Liu, Wuxing Wang, Jin Yang, Zhiwen Chen

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.7field-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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026
    Review
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  7. NR4A3 suppresses bladder cancer progression by modulating autophagyEuropean journal of histochemistry : EJH · 2025
    Article
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  9. Review
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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

10 authors at 2 institutions in 1 country.

Liwei WangUrology Institute of People's Liberation Army, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Jiazhong ShiDepartment of Cell Biology, Third Military Medical University (Army Medical University), Chongqing, China.
Sha LiuDepartment of Cell Biology, Third Military Medical University (Army Medical University), Chongqing, China.
Yaqin HuangDepartment of Cell Biology, Third Military Medical University (Army Medical University), Chongqing, China.
Hua DingUrology Institute of People's Liberation Army, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Baixiong ZhaoUrology Institute of People's Liberation Army, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Yuting LiuUrology Institute of People's Liberation Army, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Wuxing WangUrology Institute of People's Liberation Army, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Jin YangDepartment of Cell Biology, Third Military Medical University (Army Medical University), Chongqing, China.
Zhiwen ChenUrology Institute of People's Liberation Army, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
Army Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Bladder cancer (BCa) is one of the most frequent malignant tumors globally, with a significant morbidity and mortality rate. Gene expression dysregulation has been proven to play a critical role in tumorigenesis. Ras-related C3 botulinum toxin substrate3 (RAC3), which is overexpressed in several malignancies and promotes tumor progression, has been identified as an oncogene. However, RAC3 has important but not fully understood biological functions in cancer. Our research aims to reveal the new functions and potential mechanisms of RAC3 involved in BCa progression. Methods: We explored the expression level of RAC3 and its relationship with prognosis by publicly accessible BCa datasets, while the correlation of RAC3 expression with clinicopathological variables of patients was analyzed. Results: Compared with non-tumor samples, RAC3 was highly expressed in BCa and negatively correlated with prognosis. KD/OE RAC3 inhibited/promoted the proliferation and migration of BCa cells. Knockdown RAC3 caused cell cycle arrest and decreased adhesion without affecting apoptosis. Inhibition of RAC3 activates PI3K/AKT/mTOR mediated autophagy and inhibits proliferation and migration of BCa cells Conclusion: RAC3 is highly expressed in BCa. It is associated with advanced clinicopathological variables and poor prognosis. Knockdown RAC3 exerts an antitumor effect by enhancing PI3K/AKT/mTOR mediated autophagy. Targeting RAC3 and autophagy simultaneously is a potential therapeutic strategy for inhibiting BCa progression and prolonging survival.

Indexed as

autophagybladder cancermetastasisPI3K/AKT/mTORRAC3

Identifiers

PMID35847878
PMCPMC9279623
OpenAlexW4283726048

What OpenQuestion holds

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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 OpenQuestion graph.