Evidence map›Paper›PMID 35257265›Full record

ArticleApoptosis : an international journal on programmed cell death2022

Ambra1 regulates apoptosis and chemosensitivity in breast cancer cells through the Akt-FoxO1-Bim pathway.

Wei-Liang Sun, Ling-Yan He, Li Liang, Si-Yu Liu, Jie Luo, Mei-Ling Lv, Zheng-Wen Cai

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  2. CRL4International journal of biological sciences · 2026
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  17. Ambra1 in cancer: implications for clinical oncology.Apoptosis : an international journal on programmed cell death · 2022
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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

7 authors at 1 institution in 1 country.

Wei-Liang Sun *Department of Medical Oncology, the Second Affiliated Hospital of Guangxi Medical University, No. 166 Daxuedonglu Road, Nanning, 530007, Guangxi, People's Republic of China. sunweiliang@stu.gxmu.edu.cn.ORCID 0000-0002-7908-9022
Ling-Yan He *Department of Medical Oncology, the Second Affiliated Hospital of Guangxi Medical University, No. 166 Daxuedonglu Road, Nanning, 530007, Guangxi, People's Republic of China.
Li LiangDepartment of Medical Oncology, the Second Affiliated Hospital of Guangxi Medical University, No. 166 Daxuedonglu Road, Nanning, 530007, Guangxi, People's Republic of China.
Si-Yu LiuDepartment of Medical Oncology, the Second Affiliated Hospital of Guangxi Medical University, No. 166 Daxuedonglu Road, Nanning, 530007, Guangxi, People's Republic of China.
Jie LuoDepartment of Medical Oncology, the Second Affiliated Hospital of Guangxi Medical University, No. 166 Daxuedonglu Road, Nanning, 530007, Guangxi, People's Republic of China.
Mei-Ling LvDepartment of Medical Oncology, the Second Affiliated Hospital of Guangxi Medical University, No. 166 Daxuedonglu Road, Nanning, 530007, Guangxi, People's Republic of China.
Zheng-Wen CaiDepartment of Medical Oncology, the Second Affiliated Hospital of Guangxi Medical University, No. 166 Daxuedonglu Road, Nanning, 530007, Guangxi, People's Republic of China.
Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sensitivity of cells to chemotherapeutic agents has a major effect on disease outcome in breast cancer patients. Unfortunately, there are numerous factors involved in the regulation of chemosensitivity, and the mechanisms need to be further investigated. Autophagy/Beclin 1 regulator 1 (Ambra1) is a key protein in the crosstalk between autophagy and apoptosis. It controls the switch between these two processes, which determines whether cells survive or die. Induction of apoptosis is the primary mechanism by which most chemotherapeutic drugs eliminate cancer cells. Recently, Ambra1 has been shown to modulate paclitaxel-induced apoptosis in breast cancer cells via the Bim/mitochondrial pathway, thereby modifying the sensitivity of cells to paclitaxel. However, how Ambra1 regulates Bim expression remains unclear. Here, we further confirmed that Bim plays an indispensable role in Ambra1's regulation of apoptosis and chemosensitivity in breast cancer cells. Furthermore, Ambra1 was found to regulate Bim expression at the transcriptional level through the Akt-FoxO1 pathway. Therefore, we propose a novel pathway, Ambra1-Akt-FoxO1-Bim, which regulates apoptosis and chemosensitivity in breast cancer cells. Thus, Ambra1 may represent a potential target for breast cancer treatment.

Indexed as

ApoptosisBreast NeoplasmsAdaptor Proteins, Signal TransducingFemaleForkhead Box Protein O1HumansPaclitaxelProto-Oncogene Proteins c-aktAdaptor Proteins, Signal TransducingAMBRA1 protein, humanForkhead Box Protein O1FOXO1 protein, humanPaclitaxelProto-Oncogene Proteins c-aktAmbra1ApoptosisBimBreast cancerChemotherapyFoxO1

Identifiers

PMID35257265
OpenAlexW4220984657

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Registered trials

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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.