Evidence map›Paper›PMID 31649843›Full record

ArticleActa pharmaceutica Sinica. B2019

Inactivation of TFEB and NF-

Huanmin Niu, Lilin Qian, Bin Sun, Wenjian Liu, Fang Wang, Qian Wang, Xiaotian Ji, Yanhai Luo, Effat Un Nesa, Hongxiang Lou and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Endoplasmic Reticulum Calcium Pumps and Tumor Cell Differentiation.International journal of molecular sciences · 2020
    Review
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

11 authors.

Huanmin NiuInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.
Lilin QianInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.
Bin SunKey Laboratory of Natural Products & Chemical Biology, Ministry of Education, Department of Natural Products Chemistry, School of Pharmaceutical Sciences, Shandong University, Jinan 250012, China.
Wenjian LiuInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.
Fang WangInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.
Qian WangInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.
Xiaotian JiInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.
Yanhai LuoInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.
Effat Un NesaDepartment of Radiation Oncology, Qilu Hospital of Shandong University, Jinan 250012, China.
Hongxiang LouKey Laboratory of Natural Products & Chemical Biology, Ministry of Education, Department of Natural Products Chemistry, School of Pharmaceutical Sciences, Shandong University, Jinan 250012, China.
Huiqing YuanInstitute of Medical Sciences/Department of Biochemistry and Molecular Biology, the Second Hospital of Shandong University, Jinan 250033, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is critical to regulate the senescence-associated secretory phenotype (SASP) due to its effect on promoting malignant phenotypes and limiting the efficiency of cancer therapy. In this study, we demonstrated that marchantin M (Mar-M, a naturally occurring bisbibenzyl) suppressed pro-inflammatory SASP components which were elevated in chemotherapy-resistant cells. Mar-M treatment attenuated the pro-tumorigenic effects of SASP and enhanced survival in drug-resistant mouse models. No toxicity was detected on normal fibroblast cells or in animals following this treatment. Inactivation of transcription factor EB (TFEB) and nuclear factor-

Indexed as

ALT, glutamic-pyruvic transaminaseAST, transaminaseBUN, blood urea nitrogenCDDP, cisplatinCI, combinatory indexCM, conditioned mediaCREA, creatinineCT-like, both chymotrypsin-likeDMSO, dimethyl sulfoxideDoc, docetaxelDoxo, doxorubicinDrug resistanceEdU, 5-ethynyl-2′-deoxyuridineLPS, lipopolysaccharideMarchantin MMar-M, Marchantin MMTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromideNF-κBNF-κB, nuclear factor-κBPGPH, peptidylglutamyl hydrolyzingPI, propidium iodideROS, reactive oxygen speciesSASPSASP, senescence-associated secretory phenotypeSA-β-gal, senescence-associated β-galactosidaseSv, starvationTCGA, the Cancer Genome AtlasTFEBTFEB, transcription factor EBTg, thapsigargin

Identifiers

PMID31649843
PMCPMC6804491

What OpenQuestion holds

Textmetadata
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.