Evidence map›Paper›PMID 32522979›Full record

ArticleCell death & disease2020

SHQ1 is an ER stress response gene that facilitates chemotherapeutics-induced apoptosis via sensitizing ER-stress response.

Huimin Liu, Siqi Xie, Fang Fang, Dhananjaya V Kalvakolanu, Weihua Xiao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article 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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. ER stress in obesity pathogenesis and management.Trends in pharmacological sciences · 2022
    Review
  9. Article
  10. Article
  11. The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?Frontiers in cell and developmental biology · 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

5 authors at 2 institutions in 2 countries.

Huimin Liu *Department of Oncology of the First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China, 230027, Anhui, Hefei, China.
Siqi Xie *Department of Oncology of the First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China, 230027, Anhui, Hefei, China.
Fang FangDepartment of Oncology of the First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China, 230027, Anhui, Hefei, China. fangfang@mail.ustc.edu.cn.
Dhananjaya V KalvakolanuDepartment of Microbiology and Greenebaum Comprehensive Cancer Center, University of Maryland School of Medicine, Baltimore, MD, 21201, USA. dkalvako@som.umaryland.edu.
Weihua XiaoDepartment of Oncology of the First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China, 230027, Anhui, Hefei, China. xiaow@ustc.edu.cn.
University of Science and Technology of China · CNU-M Rogel Cancer Center

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SHQ1 was reported to control the biogenesis and assembly of H/ACA ribonucleoprotein particles (RNPs). It was independently isolated as a growth suppressor, GRIM1, in a genetic screen. Recent studies have indicated that SHQ1 inhibits prostate cancer growth and metastasis. SHQ1 facilitates MYC RNA splicing to promote T-acute lymphoblastic leukemia (T-ALL) development. Thus, the mechanisms of SHQ1 in cancers remain largely unknown. We report here that SHQ1 promotes tumor apoptosis and chemo-sensitivity in hepatocellular carcinoma (HCC) cells. In HCC tissues from patients, expression of SHQ1 was significantly decreased in the tumor compared to adjacent tissues. Experiments with HCC xenograft models revealed that restoring SHQ1 levels enhanced the anti-tumor activity of the endoplasmic reticulum (ER) stress inducer tunicamycin (TM) and common chemotherapy drug paclitaxel (PTX). Mechanistically, SHQ1 is an ER-stress response gene which is regulated by p50ATF6 and XBP1s through an ER stress response like element located on the SHQ1 promoter. SHQ1 interacts with the ER chaperone GRP78 to release ER sensors PERK/IRE1α/ATF6 from GRP78/ER-sensor complexes, leading to hyper-activation of unfolded protein response (UPR). In the persistent ER stress conditions of a HepG2 xenograft tumor model, SHQ1-mediated hyper-activation of ER-sensor signaling induces apoptosis. Our study thus demonstrates a SHQ1-mediated ER-stress response feedback loop that promotes tumor sensitivity to chemotherapeutics.

Indexed as

ApoptosisAnimalsAntineoplastic AgentsBinding, CompetitiveCell Line, TumorCell ProliferationEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressFemaleHeat-Shock ProteinsHumansIntracellular Signaling Peptides and ProteinsMice, Inbred BALB CMice, NudeModels, BiologicalPaclitaxelAntineoplastic AgentsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouseIntracellular Signaling Peptides and ProteinsPaclitaxelSHQ1 protein, human

Identifiers

PMID32522979
PMCPMC7286909
OpenAlexW3032963756

What OpenQuestion holds

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LicenceCC BY
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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.