Evidence map›Paper›PMID 33371351›Full record

ReviewBiomedicines2020

STAT3 and p53: Dual Target for Cancer Therapy.

Thu-Huyen Pham, Hyo-Min Park, Jinju Kim, Jin Tae Hong, Do-Young Yoon

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  18. TP53 mutations in Romanian patients with colorectal cancer.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 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

5 authors at 2 institutions in 1 country.

Thu-Huyen PhamDepartment of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Korea.ORCID 0000-0001-8717-2072
Hyo-Min ParkDepartment of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Korea.ORCID 0000-0003-3779-6682
Jinju KimDepartment of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Korea.ORCID 0000-0003-1238-1827
Jin Tae HongCollege of Pharmacy and Medical Research Center, Chungbuk National University, Chungbuk 28160, Korea.ORCID 0000-0002-6534-9575
Do-Young YoonDepartment of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Korea.ORCID 0000-0002-0154-614X
Konkuk University · KRChungbuk National University · KR

Funding

Korean government 2018R1A2B2001225
6 · The paper itself

Abstract

The tumor suppressor p53 is considered the "guardian of the genome" that can protect cells against cancer by inducing cell cycle arrest followed by cell death. However, STAT3 is constitutively activated in several human cancers and plays crucial roles in promoting cancer cell proliferation and survival. Hence, STAT3 and p53 have opposing roles in cellular pathway regulation, as activation of STAT3 upregulates the survival pathway, whereas p53 triggers the apoptotic pathway. Constitutive activation of STAT3 and gain or loss of p53 function due to mutations are the most frequent events in numerous cancer types. Several studies have reported the association of STAT3 and/or p53 mutations with drug resistance in cancer treatment. This review discusses the relationship between STAT3 and p53 status in cancer, the molecular mechanism underlying the negative regulation of p53 by STAT3, and vice versa. Moreover, it underlines prospective therapies targeting both STAT3 and p53 to enhance chemotherapeutic outcomes.

Indexed as

cancer therapydrug resistancefeedback regulationmutant p53 (mtp53)STAT3wild-type p53 (wtp53)

Identifiers

PMID33371351
PMCPMC7767392
OpenAlexW3117298572

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.