Evidence map›Paper›PMID 32774731›Full record

ArticleAmerican journal of translational research2020

Apatinib-induced NF-κB inactivation sensitizes triple-negative breast cancer cells to doxorubicin.

Dabei Tang, Jianli Ma, Zhong Chu, Xiaowei Wang, Wenhui Zhao, Qingyuan Zhang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2020. 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
1.6field-weighted citation impact, top 14% 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, 14 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

6 authors at 1 institution in 1 country.

Dabei TangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital Haping Road No. 150, Harbin, Heilongjiang Province, China.
Jianli MaDepartment of Radiotherapy, Harbin Medical University Cancer Hospital Haping Road No. 150, Harbin, Heilongjiang Province, China.
Zhong ChuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital Haping Road No. 150, Harbin, Heilongjiang Province, China.
Xiaowei WangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital Haping Road No. 150, Harbin, Heilongjiang Province, China.
Wenhui ZhaoDepartment of Medical Oncology, Harbin Medical University Cancer Hospital Haping Road No. 150, Harbin, Heilongjiang Province, China.
Qingyuan ZhangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital Haping Road No. 150, Harbin, Heilongjiang Province, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to doxorubicin (DOX) is a major clinical challenge in triple-negative breast cancer (TNBC), which is highly diverse in different patients with variable outcomes. Apatinib is a new antiangiogenic agent, which has been reported to induce apoptosis. Nevertheless, the potential role and underlying mechanisms of apatinib in reversing DOX resistance of TNBC remain unknown. This work aims to evaluate the effects of apatinib on improving the sensitivity of TNBC cells to DOX and its underlying molecular basis. Our data indicate that apatinib treatment sensitizes DOX-resistant breast cancer cells to DOX, which is accompanied by significantly increased apoptosis. Additionally, this increased induction of apoptosis is associated with an enhancement of reactive oxygen species (ROS) accumulation. Importantly, it was found that followed by DOX treatment, apatinib could inhibit NF-κB signaling pathways, which have been validated to increase ROS production and reverse DOX resistance. Moreover, our

Indexed as

ApatinibapoptosischemoresistancedoxorubicinNF-κBROS

Identifiers

PMID32774731
PMCPMC7407711
OpenAlexW3049235638

What OpenQuestion holds

Textmetadata
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.