Evidence map›Paper›PMID 33842631›Full record

ArticleAnnals of translational medicine2021

PIK3CA mutation confers resistance to chemotherapy in triple-negative breast cancer by inhibiting apoptosis and activating the PI3K/AKT/mTOR signaling pathway.

Huayu Hu, Junyong Zhu, Yuting Zhong, Rui Geng, Yashuang Ji, Qingyu Guan, Chenyan Hong, Yufan Wei, Ningning Min, Aiying Qi and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
5.1field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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  11. Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025
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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

12 authors at 3 institutions in 1 country.

Huayu HuSchool of Medicine, Nankai University, Tianjin, China.
Junyong ZhuDepartment of General Surgery, Chinese People's Liberation Army General Hospital, Beijing, China.
Yuting ZhongDepartment of General Surgery, Chinese People's Liberation Army General Hospital, Beijing, China.
Rui GengDepartment of General Surgery, Chinese People's Liberation Army General Hospital, Beijing, China.
Yashuang JiSchool of Medicine, Nankai University, Tianjin, China.
Qingyu GuanSchool of Medicine, Nankai University, Tianjin, China.
Chenyan HongSchool of Medicine, Nankai University, Tianjin, China.
Yufan WeiSchool of Medicine, Nankai University, Tianjin, China.
Ningning MinSchool of Medicine, Nankai University, Tianjin, China.
Aiying QiDepartment of General Surgery, Chinese People's Liberation Army General Hospital, Beijing, China.
Yanjun ZhangDepartment of General Surgery, Chinese People's Liberation Army General Hospital, Beijing, China.
Xiru LiDepartment of General Surgery, Chinese People's Liberation Army General Hospital, Beijing, China.
Chinese People's Liberation Army · CNPeople's Liberation Army No. 150 Hospital · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTriple-negative breast cancer (TNBC) is a malignant subtype of breast cancer, the main treatments for which are chemotherapy and surgery.

methodsTNBC cell lines (MDA-MB-231 and MDA-MB-468) with

resultsCell viability and Transwell assays showed that PIK3CA mutation promoted TNBC cell growth and conferred an enhanced migratory phenotype. Cell cycle and apoptosis assays showed that PIK3CA mutation moderately improved the proliferation ability of TNBC cells and remarkably inhibited their apoptosis. After epirubicin therapy, the proportion of early apoptotic cells decreased among cells with PIK3CA mutation. Further, xenograft tumors grew faster in NOD/SCID mice injected with mutated cell lines than in control group, suggesting that PIK3CA mutation caused chemotherapy resistance. Importantly, western blot and immunohistochemical analysis showed that cells and mouse tumors in the PIK3CA mutation groups exhibited different expression levels of apoptosis-related markers (Xiap, Bcl-2, and Caspase 3) and proteins associated with the PI3K/AKT/mTOR pathway (p110α, AKT, p-AKT, mTOR, p-mTOR, p-4E-BP1, p-p70S6K, and Pten). Moreover, prognostic analysis of 50 patients with TNBC indicated that PIK3CA mutation might be linked with relapse and death.

conclusionsPIK3CA mutation confers resistance to chemotherapy in TNBC by inhibiting apoptosis and activating the PI3K/AKT/mTOR signaling pathway.

Indexed as

apoptosischemotherapy resistancePI3K/AKT/mTOR pathwayPIK3CA mutationTriple-negative breast cancer (TNBC)

Identifiers

PMID33842631
PMCPMC8033310
OpenAlexW3139293810

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.