Evidence map›Paper›PMID 25821946›Full record

ArticleOncogenesis2015

Rap1 is indispensable for TRF2 function in etoposide-induced DNA damage response in gastric cancer cell line.

X Li, W Liu, H Wang, L Yang, Y Li, H Wen, H Ning, J Wang, L Zhang, J Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 17 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 1 country.

X LiDepartment of Neurology, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
W LiuDepartment V of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
H WangDepartment V of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
L YangDepartment V of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Y LiDepartment V of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
H WenDepartment V of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
H NingDepartment V of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
J WangDepartment V of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
L ZhangDepartment II of Digestive Diseases, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
J LiDepartment of Neurology, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
D FanState Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases, The Fourth Military Medical University, Xi'an, China.
First Affiliated Hospital of Zhengzhou University · CNSecond Affiliated Hospital of Zhengzhou University · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The telomeric protein TRF2, involving in telomeric and extratelomeric DNA damage response, has been previously reported to facilitate multidrug resistance (MDR) in gastric cancer cells by interfering ATM-dependent DNA damage response induced by anticancer drugs. Rap1 is the TRF2-interacting protein in the shelterin complex. Complex formation between Rap1 and TRF2 is essential for their function in telomere and end protection. Here we focus on the effects of Rap1 on TRF2 function in DNA damage response induced by anticancer drugs. Both Rap1 and TRF2 expression were upregulated in SGC7901 and its MDR variant SGC7901/VCR after etoposide treatment, which was more marked in SGC7901/VCR than in SGC7901. Rap1 silencing by siRNA in SGC7901/VCR partially reversed the etoposide resistance. And Rap1 silencing partially reversed the TRF2-mediated resistance to etoposide in SGC7901. Rap1 silencing did not affect the TRF2 upregulation induced by etoposide, but eliminated the inhibition effect of TRF2 on ATM expression and ATM phosphorylation at serine 1981 (ATM pS1981). Furthermore, phosphorylation of ATM targets, including γH2AX and serine 15 (S15) on p53, were increased in Rap1 silencing cells in response to etoposide. Thus, we confirm that Rap1, interacting with TRF2 in the shelterin complex, also has an important role in TRF2-mediated DNA damage response in gastric cancer cells treated by etoposide.

Identifiers

PMID25821946
PMCPMC4491608
OpenAlexW1984267333

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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.