Evidence map›Paper›PMID 26810068›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

GRIM-19 inhibition induced autophagy through activation of ERK and HIF-1α not STAT3 in Hela cells.

Xin Yue, Peiwei Zhao, Kongming Wu, Juan Huang, Wen Zhang, Yaogui Wu, Xiaohui Liang, Xuelian He

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Xin YueClinical Research Center, Wuhan Medical and Healthcare Center for Women and Children, No. 100 Hongkong Rd, Wuhan, Hubei, China.
Peiwei ZhaoClinical Research Center, Wuhan Medical and Healthcare Center for Women and Children, No. 100 Hongkong Rd, Wuhan, Hubei, China.
Kongming WuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, China.
Juan HuangDepartment of Pathology, Wuhan Medical and Healthcare Center for Women and Children, Wuhan, Hubei, China.
Wen ZhangDepartment of Pathology, Wuhan Medical and Healthcare Center for Women and Children, Wuhan, Hubei, China.
Yaogui WuSchool of Public Health, Wuhan University, Wuhan, China.
Xiaohui LiangDepartment of Oncology, Renmin Hospital, Wuhan University, Wuhan, China.
Xuelian HeClinical Research Center, Wuhan Medical and Healthcare Center for Women and Children, No. 100 Hongkong Rd, Wuhan, Hubei, China. hexuelian2013@hotmail.com.
Wuhan Medical Center for Women and Children · CNWuhan University · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene associated with retinoid-interferon-induced mortality (GRIM-19), an important subunit of mitochondrial complex I, has been identified as a tumor suppressor, and its reduced expression has been reported to be associated with tumorigenesis and metastasis. Autophagy has been proposed as a protective mechanism for cell survival under various stresses, including chemotherapy. However, it remains unknown whether GRIM-19 is linked to autophagy and chemotherapy resistance. Here, we showed that suppression of GRIM-19 by shRNA enhanced cell-type-dependent autophagy by activating extracellular regulated protein kinase (ERK) and hypoxia inducible factor-1a (HIF-1a) in a reactive oxygen species (ROS)-mediated manner, and thereby conferred resistance to paclitaxel. Besides, the antioxidant N-acetyl-L-cysteine (NAC) and autophagy inhibitor 3-MA could in part overcome this resistance. We also found that GRIM-19 expression was significantly correlated with clinical stage and grade in patients with cervical cancers. Taken together, our results indicated that GRIM-19 inhibition induced autophagy and chemotherapy resistance, which could affect prognosis of cervical cancers. Our study has identified new function of GRIM-19 and its underlying mechanism, and it will provide possible avenues for therapeutic targeting in cervical cancers.

Indexed as

AdultAntineoplastic Agents, PhytogenicApoptosisApoptosis Regulatory ProteinsAutophagyBiomarkers, TumorBlotting, WesternCase-Control StudiesCell ProliferationDrug Resistance, NeoplasmFemaleFluorescent Antibody TechniqueFollow-Up StudiesHeLa CellsHumansHypoxia-Inducible Factor 1, alpha SubunitAntineoplastic Agents, PhytogenicApoptosis Regulatory ProteinsBiomarkers, TumorHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADH, NADPH OxidoreductasesNDUFA13 protein, humanPaclitaxelRNA, Small InterferingSTAT3 protein, humanSTAT3 Transcription FactorAutophagyCervical cancerChemotherapyERKGRIM-19HIF-1a

Identifiers

PMID26810068
OpenAlexW2270107748

What OpenQuestion holds

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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.