Evidence map›Paper›PMID 26474277›Full record

ArticleOncotarget2015

Involvement of Wnt/β-catenin signaling in the mesenchymal stem cells promote metastatic growth and chemoresistance of cholangiocarcinoma.

Weiwei Wang, Wei Zhong, Jiahui Yuan, Congcong Yan, Shaoping Hu, Yinping Tong, Yubin Mao, Tianhui Hu, Bing Zhang, Gang Song

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Molecular Targets and Signaling Pathways in Cholangiocarcinoma: A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2023
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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 1 institution in 1 country.

Weiwei WangCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Wei ZhongCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Jiahui YuanCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Congcong YanCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Shaoping HuCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Yinping TongCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Yubin MaoDepartment of Basic Medicine, Medical College of Xiamen University, Xiamen 361102, China.
Tianhui HuCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Bing ZhangDepartment of Basic Medicine, Medical College of Xiamen University, Xiamen 361102, China.
Gang SongCancer Research Center, Medical College of Xiamen University, Xiamen 361102, China.
Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) are multi-potent progenitor cells with ability to differentiate into multiple lineages, including bone, cartilage, fat, and muscles. Recent research indicates that MSCs can be efficiently recruited to tumor sites, modulating tumor growth and metastasis. However, the underlying molecular mechanisms are not fully understood. Here, we first demonstrated that human umbilical cord-derived mesenchymal stem cells (hUC-MSCs), when mixed with human cholangiocarcinoma cell lines QBC939 in a xenograft tumor model, significantly increased the cancer cells proliferation and metastatic potency. MSCs and their conditioned media (MSC-CM) could improve the drug resistance of tumor when the compound K (CK) as an anti-cancer drug, a major intestinal bacterial metabolite of panaxoside, was administered to xenograft tumor mice. Furthermore, MSCs greatly increased the colony formation and invasion of cholangiocarcinoma cells QBC939 and Mz-ChA-1. Immunochemistry studies of cholangiocarcinoma tissue chips and transplantation tumor from nude mice showed that the expression of β-catenin was important for cholangiocarcinoma development. We further demonstrated that MSCs and MSCs-CM could promote proliferation and migration of cholangiocarcinoma cells through targeting the Wnt/β-catenin signaling pathway. hUC-MSCs or MSCs-CM stimulated Wnt activity by promoting the nuclear translocation of β-catenin, and up-regulated Wnt target genes MMPs family, cyclin D1 and c-Myc. Together, our studies highlight a critical role for MSCs on cancer metastasis and indicate MSCs promote metastatic growth and chemoresistance of cholangiocarcinoma cells via activation of Wnt/β-catenin signaling.

Indexed as

AnimalsApoptosisBile Duct NeoplasmsBlotting, WesternCell Line, TumorCell ProliferationCells, CulturedCholangiocarcinomaCulture Media, ConditionedDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGinsenosidesHumansMaleMesenchymal Stem CellsMice, Inbred BALB CCulture Media, Conditionedginsenoside compound KGinsenosideschemoresistancecholangiocarcinomametastasisMSCsβ-catenin

Identifiers

PMID26474277
PMCPMC4747224
OpenAlexW2173594285

What OpenQuestion holds

Textmetadata
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.