Evidence map›Paper›PMID 26540347›Full record

ArticleOncotarget2015

Knock out CD44 in reprogrammed liver cancer cell C3A increases CSCs stemness and promotes differentiation.

Shuo Han, Jinhai Guo, Yinan Liu, Zhi Zhang, Qihua He, Peng Li, Mingzhi Zhang, Haojie Sun, Ruizhi Li, Yang Li and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 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

15 authors at 3 institutions in 1 country.

Shuo HanDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Jinhai GuoBeijing DongFang YaMei Gene Science and Technology Research Institute, Beijing, People's Republic of China.
Yinan LiuDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Zhi ZhangState Key Laboratory of Organ Failure Research, Co-Innovation Center for Organ Failure Research, Guangdong Provincial Research Center of Artificial Organ and Tissue Engineering, Second Department of Hepatobiliary Surgery, ZhuJiang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Qihua HeDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Peng LiDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Mingzhi ZhangDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Haojie SunDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Ruizhi LiDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Yang LiState Key Laboratory of Organ Failure Research, Co-Innovation Center for Organ Failure Research, Guangdong Provincial Research Center of Artificial Organ and Tissue Engineering, Second Department of Hepatobiliary Surgery, ZhuJiang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Wotan ZengBeijing DongFang YaMei Gene Science and Technology Research Institute, Beijing, People's Republic of China.
Jinwen LiuBeijing DongFang YaMei Gene Science and Technology Research Institute, Beijing, People's Republic of China.
Lejian LianBeijing DongFang YaMei Gene Science and Technology Research Institute, Beijing, People's Republic of China.
Yi GaoState Key Laboratory of Organ Failure Research, Co-Innovation Center for Organ Failure Research, Guangdong Provincial Research Center of Artificial Organ and Tissue Engineering, Second Department of Hepatobiliary Surgery, ZhuJiang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Li ShenDepartment of Cell Biology, Stem Cell Research Center, Department of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Peking University · CNSouthern Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD44 is a widely known cancer stem cells marker in various cancers and validated to function in tumor growth, survival and tumor metastasis. In this study, we first established C3A-derived liver cancer stem cells by OSKM method [OCT4, SOX2, KLF4, and c-MYC], termed C3A-induced cancer stem cells (C3A-iCSCs) which acquired self-renewal and stemness abilities. Then we found CD44 was positive in C3A-iCSCs and mainly located in cell nuclear. Chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) results showed nuclear CD44 combined promoter regions of c-MYC and SOX2. These results suggested that CD44 participated in C3A-iCSCs transcriptional regulation. To explore CD44 overall influence in liver cancer stem cells, CD44 was knocked out in C3A-iCSCs using CRISPR/Cas9 technology. Our results showed a dramatic increase in the expression of stem cell markers OCT4, SOX2 and NANOG in CD44- C3A-iCSCs compared with that in CD44+ C3A-iCSCs. Tumor derived from CD44- C3A-iCSCs also displayed well-differentiated tumor cells compared to CD44+ C3A-iCSCs, which suggested CD44- C3A-iCSCs derived tumor cells exhibited lower malignant degree. Our data indicated nuclear CD44 in liver cancer stem cells is responsible for the poorly differentiated highly malignant tumor cells by maintenance of low stemness state.

Indexed as

Cell DifferentiationCellular ReprogrammingCellular Reprogramming TechniquesGene Knockout TechniquesBinding SitesBiomarkers, TumorCarcinoma, HepatocellularCell NucleusCRISPR-Cas SystemsGene Expression Regulation, NeoplasticGenotypeHep G2 CellsHomeodomain ProteinsHumansHyaluronan ReceptorsKruppel-Like Factor 4Biomarkers, TumorCD44 protein, humanHomeodomain ProteinsHyaluronan ReceptorsKLF4 protein, humanKruppel-Like Factor 4MYC protein, humanNanog Homeobox ProteinNANOG protein, humanProto-Oncogene Proteins c-mycSOX2 protein, humanSOXB1 Transcription FactorsC3ACD44CRISPR/Cas9induced liver cancer stem cellstranscriptional regulation

Identifiers

PMID26540347
PMCPMC4792568
OpenAlexW2114951727

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.