Evidence map›Paper›PMID 32875699›Full record

ArticleCancer science2020

Complex roles of the actin-binding protein Girdin/GIV in DNA damage-induced apoptosis of cancer cells.

Chen Chen, Atsushi Enomoto, Liang Weng, Tetsuro Taki, Yukihiro Shiraki, Shinji Mii, Ryosuke Ichihara, Mitsuro Kanda, Masahiko Koike, Yasuhiro Kodera and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 11 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

11 authors at 3 institutions in 2 countries.

Chen ChenDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0002-9206-6116
Liang WengCenter for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Tetsuro TakiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0001-8654-6896
Yukihiro ShirakiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shinji MiiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0001-8266-3235
Ryosuke IchiharaDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Mitsuro KandaDepartment of Gastroenterological Surgery (Surgery II), Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masahiko KoikeDepartment of Gastroenterological Surgery (Surgery II), Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yasuhiro KoderaDepartment of Gastroenterological Surgery (Surgery II), Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masahide TakahashiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0002-2803-2683
Nagoya University · JPCentral South University · CNFujita Health University · JP

Funding

Japan Agency for Medical Research and Development 19cm0106332h0002Japan Agency for Medical Research and Development 19gm0810007h0104Japan Agency for Medical Research and Development 19gm1210008s0101Ministry of Education, Culture, Sports, Science and Technology of Japan 18H02638Ministry of Education, Culture, Sports, Science and Technology of Japan 26221304
6 · The paper itself

Abstract

The actin-binding protein Girdin is a hub protein that interacts with multiple proteins to regulate motility and Akt and trimeric G protein signaling in cancer cells. Girdin expression correlates with poor outcomes in multiple human cancers. However, those findings are not universal, as they depend on study conditions. Those data suggest that multiple aspects of Girdin function and its role in tumor cell responses to anticancer therapeutics must be reconsidered. In the present study, we found that Girdin is involved in DNA damage-induced cancer cell apoptosis. An esophageal cancer cell line that exhibited high Girdin expression showed a marked sensitivity to UV-mediated DNA damage compared to a line with low Girdin expression. When transcriptional activation of endogenous Girdin was mediated by an engineered CRISPR/Cas9 activation system, sensitivity to DNA damage increased in both stationary and migrating HeLa cancer cells. High Girdin expression was associated with dysregulated cell cycle progression and prolonged G

Indexed as

DNA DamageAgedAged, 80 and overAnimalsApoptosisBiomarkersCell CycleCell Line, TumorEsophageal NeoplasmsFemaleHeLa CellsHumansMaleMicrofilament ProteinsMiddle AgedMitosisBiomarkersCCDC88A protein, humanMicrofilament ProteinsVesicular Transport Proteinsapoptosiscancer cell heterogeneitycell cyclecell migrationDNA damageGirdin

Identifiers

PMID32875699
PMCPMC7648047
OpenAlexW3082243188

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.