Evidence map›Paper›PMID 28192613›Full record

ArticleCancer science2017

SNIPER(TACC3) induces cytoplasmic vacuolization and sensitizes cancer cells to Bortezomib.

Nobumichi Ohoka, Katsunori Nagai, Norihito Shibata, Takayuki Hattori, Hiroshi Nara, Nobuo Cho, Mikihiko Naito

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  9. Targeted protein degradation: elements of PROTAC design.Current opinion in chemical biology · 2019
    Review
  10. The PROTAC technology in drug development.Cell biochemistry and function · 2019
    Review
  11. Article
  12. Article
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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

7 authors at 2 institutions in 1 country.

Nobumichi OhokaDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Setagaya-ku, Tokyo, Japan.
Katsunori NagaiMedicinal Chemistry Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Co. Ltd., Fujisawa, Kanagawa, Japan.
Norihito ShibataDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Setagaya-ku, Tokyo, Japan.
Takayuki HattoriDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Setagaya-ku, Tokyo, Japan.
Hiroshi NaraMedicinal Chemistry Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Co. Ltd., Fujisawa, Kanagawa, Japan.
Nobuo ChoMedicinal Chemistry Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Co. Ltd., Fujisawa, Kanagawa, Japan.
Mikihiko NaitoDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Setagaya-ku, Tokyo, Japan.ORCID http://orcid.org/0000-0003-0451-1337
National Institute of Health Sciences · JPTakeda (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously developed a hybrid small molecule SNIPER (Specific and Nongenetic IAP-dependent Protein ERaser) against transforming acidic coiled-coil-3 (TACC3), SNIPER(TACC3), that induces proteasomal degradation of TACC3 protein. In this study, we found that SNIPER(TACC3) induces cytoplasmic vacuolization derived from endoplasmic reticulum (ER) and paraptosis-like cell death selectively in cancer cells. Mechanistic analysis suggests that accumulation of ubiquitylated protein aggregates that requires X-linked inhibitor of apoptosis protein (XIAP) induces ER stress, which results in ER-stress responses involving X-box binding protein-1 (XBP-1) and ER-derived vacuolization in cancer cells. Importantly, inhibition of proteasome enhanced the SNIPER(TACC3)-induced vacuolization, and the combination treatment of SNIPER(TACC3) and bortezomib exhibited a synergistic anticancer activity in several cancer cell lines. The induction of paraptosis-like cell death in cancer cells by SNIPER(TACC3) could be applied to treat cancer cells resistant to undergo apoptosis by overexpression of XIAP.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsApoptosisBortezomibCell DeathCell Line, TumorCytoplasmDrug SynergismEndoplasmic ReticulumEndoplasmic Reticulum StressHumansK562 CellsMCF-7 CellsMicrotubule-Associated ProteinsProteasome Endopeptidase ComplexSmall Molecule LibrariesX-Linked Inhibitor of Apoptosis ProteinBortezomibMicrotubule-Associated ProteinsProteasome Endopeptidase ComplexSmall Molecule LibrariesTACC3 protein, humanX-Linked Inhibitor of Apoptosis ProteinBortezomibcytoplasmic vacuolizationparaptosisSNIPER(TACC3)XIAP

Identifiers

PMID28192613
PMCPMC5448626
OpenAlexW2588248436

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.