Evidence map›Paper›PMID 39419941›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2024

USP28 promotes tumor progression and glycolysis by stabilizing PKM2/Hif1-α in cholangiocarcinoma.

Qian Qiao, Jifei Wang, Shuochen Liu, Jiang Chang, Tao Zhou, Changxian Li, Yaodong Zhang, Wangjie Jiang, Yananlan Chen, Xiao Xu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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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

12 authors.

Qian Qiao *Department of Hepatobiliary Surgery, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu Province, China.
Jifei Wang *Hepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Shuochen Liu *Hepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Jiang ChangHepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Tao ZhouHepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Changxian LiHepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Yaodong ZhangHepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Wangjie JiangHepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Yananlan ChenHepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Xiao XuHepatobiliary Center, Key Laboratory of Liver Transplantation, The First Affiliated Hospital of Nanjing Medical University, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Mingyu WuDepartment of Hepatobiliary Surgery, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu Province, China. wumingyuqaz1234@163.com.
Xiangcheng LiDepartment of Hepatobiliary Surgery, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu Province, China. drxcli@njmu.edu.cn.

Funding

the Key Project of Wuxi Medical Center WXKY202303002the Key Research and Development Program of Jiangsu Province BE2016789the National Natural Science Foundation Project 82273066
6 · The paper itself

Abstract

backgroundUbiquitination is one of the important modification of proteins which can be reversed by deubiquitinating enzymes (DUBs). Ubiquitin specific protease 28 (USP28) belongs to the deubiquitinase family, which plays a cancer-promoting function in many types of cancers such as pancreatic cancer and breast cancer. So far, the molecular function and significance of USP 28 in cholangiocarcinoma remain unclear.

methodsIn this study, we evaluated the expression of USP28 using tissue microarray (TMA), reverse transcription polymerase chain reaction (qRT-PCR), and online databases. We investigated the effect of USP28 on the progression of CCA through in vitro and in vivo functional experiments. In addition, we explored downstream molecular pathways using Western blotting (WB), immunofluorescence (IF), and mass spectrometry techniques.

resultsHere, we found that cholangiocarcinoma tissue had higher USP 28 expression than normal bile duct tissue, and that high USP 28 levels were significantly associated with a malignant phenotype and poorer prognosis in cholangiocarcinoma patients. Both in vitro and in vivo, USP28 could mediate the deubiquitination of PKM2, thereby activating the downstream Hif1-α signaling pathway, promoting glycolysis and energy supply, and finally promoting tumor progression.

conclusionIn summary, USP28 activated downstream Hif1-α by reducing the ubiquitination level of PKM2, furthermore, promoting the level of glycolysis in CCA cells for tumor progression.

Indexed as

Bile Duct NeoplasmsCarrier ProteinsCholangiocarcinomaDisease ProgressionGlycolysisHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsMice, NudeThyroid Hormone-Binding ProteinsThyroid HormonesUbiquitin ThiolesteraseAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansCarrier ProteinsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsThyroid Hormone-Binding ProteinsThyroid HormonesUbiquitin ThiolesteraseUSP28 protein, humanCholangiocarcinomaHif1-αPKM2UbiquitinationUSP28

Identifiers

PMID39419941
PMCPMC12973973

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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.