Evidence map›Paper›PMID 27363028›Full record

ArticleOncotarget2016

CD147 knockdown improves the antitumor efficacy of trastuzumab in HER2-positive breast cancer cells.

Lijuan Xiong, Li Ding, Haoyong Ning, Chenglin Wu, Kaifei Fu, Yuxiao Wang, Yan Zhang, Yan Liu, Lijun Zhou

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Cyclophilin A/CD147 Interaction: A Promising Target for Anticancer Therapy.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
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

9 authors at 2 institutions in 1 country.

Lijuan XiongCentral Laboratory, Navy General Hospital, Beijing 100048, P.R. China.
Li DingThe Third School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, 510630, P.R.China.
Haoyong NingDepartment of Pathology, Navy General Hospital, Beijing 100048, P.R. China.
Chenglin WuCentral Laboratory, Navy General Hospital, Beijing 100048, P.R. China.
Kaifei FuCentral Laboratory, Navy General Hospital, Beijing 100048, P.R. China.
Yuxiao WangCentral Laboratory, Navy General Hospital, Beijing 100048, P.R. China.
Yan ZhangDepartment of Surgery, Navy General Hospital, Beijing 100048, P.R. China.
Yan LiuThe Third School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, 510630, P.R.China.
Lijun ZhouCentral Laboratory, Navy General Hospital, Beijing 100048, P.R. China.
PLA Navy General Hospital · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trastuzumab is widely used in the clinical treatment of human epidermal growth factor receptor-2 (HER2)-positive breast cancer, but the patient response rate is low. CD147 stimulates cancer cell proliferation, migration, metastasis and differentiation and is involved in chemoresistance in many types of cancer cells. Whether CD147 alters the effect of trastuzumab on HER2-positive breast cancer cells has not been previously reported. Our study confirmed that CD147 suppression enhances the effects of trastuzumab both in vitro and in vivo. CD147 suppression increased the inhibitory rate of trastuzumab and cell apoptosis in SKBR3, BT474, HCC1954 and MDA-MB453 cells compared with the controls. Furthermore, CD147 knockdown increased expression of cleaved Caspase-3/9 and poly (ADP-ribose) polymerase (PARP) and decreased both mitogen-activated protein kinase (MAPK) and Akt phosphorylation in the four cell lines. In an HCC1954 xenograft model, trastuzumab achieved greater suppression of tumor growth in the CD147-knockdown group than in the shRNA negative control (NC) group. These data indicated that enhancement of the effect of trastuzumab on HER2-positive cells following CD147 knockdown might be attributed to increased apoptosis and decreased phosphorylation of signaling proteins. CD147 may be a key protein for enhancing the clinical efficacy of trastuzumab.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic Agents, ImmunologicalApoptosisBasiginBreast NeoplasmsCell DifferentiationCell Line, TumorCell MovementCell ProliferationCell SurvivalErb-b2 Receptor Tyrosine KinasesFemaleHumansMiceMice, Inbred BALB CAntineoplastic Agents, ImmunologicalBasiginBSG protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesPoly(ADP-ribose) PolymerasesRNA, Small InterferingTrastuzumabantibody drug resistance/sensitivitybreast cancerCD147HER2trastuzumab efficacy

Identifiers

PMID27363028
PMCPMC5295386
OpenAlexW2475165174

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.