Evidence map›Paper›PMID 29573636›Full record

ArticleNeoplasia (New York, N.Y.)2018

POH1 Knockdown Induces Cancer Cell Apoptosis via p53 and Bim.

Chun-Hua Wang, Shi-Xun Lu, Li-Li Liu, Yong Li, Xia Yang, Yang-Fan He, Shi-Lu Chen, Shao-Hang Cai, Hong Wang, Jing-Ping Yun

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2018. 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
2.2field-weighted citation impact, top 12% 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, 36 citations in OpenAlex.

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  11. Research progress on proteasome subunits in regulating occurrence and development of hepatocellular carcinoma.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  12. Small-Molecule Inhibitors Targeting Proteasome-Associated Deubiquitinases.International journal of molecular sciences · 2021
    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 3 institutions in 1 country.

Chun-Hua WangSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: wangchunh@sysucc.org.cn.
Shi-Xun LuSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: lushix@sysucc.org.cn.
Li-Li LiuSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: liulil@sysucc.org.cn.
Yong LiSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: liyong@sysucc.org.cn.
Xia YangSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: yangxia1@sysucc.org.cn.
Yang-Fan HeSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: heyangf@sysucc.org.cn.
Shi-Lu ChenSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: chenshil@sysucc.org.cn.
Shao-Hang CaiSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: caishaoh@sysucc.org.cn.
Hong WangSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: wanghong@sysucc.org.cn.
Jing-Ping YunSun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, 651# Dong Feng Road East, Guangzhou 510060, China; Department of Pathology, Sun Yat-sen University Cancer Center, 651# Dong Feng Road East, Guangzhou 510060, China. Electronic address: yun_lab@hotmail.com.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNState Key Laboratory of Oncology in South China

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ubiquitin-proteasome system is implicated in cell apoptosis that is frequently dysregulated in human cancers. POH1/rpn11/PSMD14, as a part of the 19S proteasomal subunit, contributes to the progression of malignancy, but its role in apoptosis remains unclear. Here, we showed that POH1 expression was increased and associated with poor outcomes in three independent cohorts of patients with hepatocellular carcinoma (HCC), esophageal cancer (EC), and colorectal cancer (CRC). The knockdown of POH1 significantly inhibited tumor cell proliferation and induced apoptosis mediated by the mitochondrial pathway in vitro. Intratumoral injection of POH1 small interfering RNA (siRNA) significantly reduced the progression of tumor growth and induced apoptosis in vivo. Furthermore, p53 or Bim siRNA markedly attenuated the apoptosis induced by POH1 depletion. POH1 depletion resulted in cell apoptosis by increasing the stability of p53 and Bim and inhibiting their ubiquitination. Overall, POH1 knockdown induced cell apoptosis through increased expression of p53 and Bim via enhanced protein stability and attenuated degradation. Thus, POH1 may serve as a potential prognostic marker and therapeutic target in human cancers.

Indexed as

AnimalsApoptosisBcl-2-Like Protein 11Cell Line, TumorCell ProliferationHCT116 CellsHumansMaleMiceMice, Inbred BALB CMice, NudeNeoplasmsProteasome Endopeptidase ComplexRNA, Small InterferingTrans-ActivatorsTumor Suppressor Protein p53Bcl-2-Like Protein 11Proteasome Endopeptidase ComplexPSMD14 protein, humanRNA, Small InterferingTP53 protein, humanTrans-ActivatorsTumor Suppressor Protein p53Ubiquitin

Identifiers

PMID29573636
PMCPMC5915990
OpenAlexW2789451531

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.