Evidence map›Paper›PMID 29160412›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2017

Exosomes promote cetuximab resistance via the PTEN/Akt pathway in colon cancer cells.

S Zhang, Y Zhang, J Qu, X Che, Y Fan, K Hou, T Guo, G Deng, N Song, C Li and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  9. Review
  10. Exosomes in metastasis of colorectal cancers: Friends or foes?World journal of gastrointestinal oncology · 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

13 authors at 2 institutions in 1 country.

S ZhangDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
Y ZhangDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
J QuDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
X CheDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
Y FanDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
K HouDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
T GuoDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
G DengDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
N SongDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
C LiDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
X WanDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
X QuDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
Y LiuDepartment of Medical Oncology, the First Hospital of China Medical University, Shenyang, China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cetuximab is widely used in patients with metastatic colon cancer expressing wildtype KRAS. However, acquired drug resistance limits its clinical efficacy. Exosomes are nanosized vesicles secreted by various cell types. Tumor cell-derived exosomes participate in many biological processes, including tumor invasion, metastasis, and drug resistance. In this study, exosomes derived from cetuximab-resistant RKO colon cancer cells induced cetuximab resistance in cetuximab-sensitive Caco-2 cells. Meanwhile, exosomes from RKO and Caco-2 cells showed different levels of phosphatase and tensin homolog (PTEN) and phosphor-Akt. Furthermore, reduced PTEN and increased phosphorylated Akt levels were found in Caco-2 cells after exposure to RKO cell-derived exosomes. Moreover, an Akt inhibitor prevented RKO cell-derived exosome-induced drug resistance in Caco-2 cells. These findings provide novel evidence that exosomes derived from cetuximab-resistant cells could induce cetuximab resistance in cetuximab-sensitive cells, by downregulating PTEN and increasing phosphorylated Akt levels.

Indexed as

Analysis of VarianceAntineoplastic Agents, ImmunologicalBlotting, WesternCaco-2 CellsCell Line, TumorCell SurvivalCetuximabColonic NeoplasmsDrug ResistanceExosomesFormazansHumansProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTetrazolium SaltsTime FactorsAntineoplastic Agents, ImmunologicalCetuximabFormazansMTT formazanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTetrazolium Salts

Identifiers

PMID29160412
PMCPMC5685060
OpenAlexW2767862821

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.