Evidence map›Paper›PMID 32973135›Full record

ReviewCell death & disease2020

PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers.

Rui Liu, Youwen Chen, Guangzhi Liu, Chenxi Li, Yurong Song, Zhiwen Cao, Wen Li, Jinghong Hu, Cheng Lu, Yuanyan Liu

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 527 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
527citing papers in PubMed, 1 pooled it
36.4field-weighted citation impact, top 1% 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

527 citing papers in PubMed, 1 synthesis or guideline pooled it, 893 citations in OpenAlex.

  1. Pooled it
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  3. Mutant p53Molecular oncology · 2026
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  18. Antioxidants (Basel, Switzerland) · 2026
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467 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Rui LiuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.
Youwen ChenSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.
Guangzhi LiuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.
Chenxi LiSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.
Yurong SongSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.
Zhiwen CaoSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.
Wen LiSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.
Jinghong HuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China. hujhbj@163.com.
Cheng LuInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, 100700, Beijing, China. lv_cheng0816@163.com.
Yuanyan LiuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China. yyliu_1980@163.com.
Beijing University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance (MDR) is the dominant challenge in the failure of chemotherapy in cancers. Phosphatidylinositol 3-kinase (PI3K) is a lipid kinase that spreads intracellular signal cascades and regulates a variety of cellular processes. PI3Ks are considered significant causes of chemoresistance in cancer therapy. Protein kinase B (AKT) is also a significant downstream effecter of PI3K signaling, and it modulates several pathways, including inhibition of apoptosis, stimulation of cell growth, and modulation of cellular metabolism. This review highlights the aberrant activation of PI3K/AKT as a key link that modulates MDR. We summarize the regulation of numerous major targets correlated with the PI3K/AKT pathway, which is further related to MDR, including the expression of apoptosis-related protein, ABC transport and glycogen synthase kinase-3 beta (GSK-3β), synergism with nuclear factor kappa beta (NF-κB) and mammalian target of rapamycin (mTOR), and the regulation of glycolysis.

Indexed as

Cell ProliferationDrug Resistance, MultipleHumansNeoplasmsProto-Oncogene Proteins c-aktSignal TransductionProto-Oncogene Proteins c-akt

Identifiers

PMID32973135
PMCPMC7515865
OpenAlexW3088838661

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.