Evidence map›Paper›PMID 35110552›Full record

ArticleCell death & disease2022

The feedback loop of ANKHD1/lncRNA MALAT1/YAP1 strengthens the radioresistance of CRC by activating YAP1/AKT signaling.

Ping-An Yao, Yong Wu, Kui Zhao, Yecheng Li, Jianping Cao, Chungen Xing

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Radiotherapy effects on the ceRNA network in high-risk prostate cancer patients.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025
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  18. METTL3 Mediates Epithelial-Mesenchymal Transition by Modulating FOXO1 mRNA NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
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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

6 authors at 1 institution in 1 country.

Ping-An Yao *Department of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Yong Wu *Department of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Kui ZhaoDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Yecheng LiDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Jianping CaoSchool of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, 215123, China. jpcao@suda.edu.cn.ORCID 0000-0003-0395-8436
Chungen XingDepartment of General Surgery, Second Affiliated Hospital of Soochow University, Suzhou, 215004, China. xingcg@suda.edu.cn.ORCID 0000-0001-7865-1258
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate radioresistance substantially limits the effectiveness of radiotherapy for colorectal cancer (CRC); thus, a strategy to enhance the radiosensitivity of CRC is urgently needed. Herein, we reported that ankyrin repeat and KH domain containing 1 (ANKHD1) serves as a key regulator of radioresistance in CRC. ANKHD1 was highly expressed in CRC tissues and was highly correlated with Yes-associated protein 1 (YAP1) in CRC. Our results first revealed that ANKHD1 knockdown could increase the radiosensitivity of CRC by regulating DNA-damage repair, both in vitro and in vivo. Furthermore, the interactive regulation between ANKHD1 or YAP1 and lncRNA MALAT1 was revealed by RIP and RNA pull-down assays. Moreover, our results also demonstrated that MALAT1 silencing can radiosensitize CRC cells to IR through YAP1/AKT axis, similar to ANKHD1 silencing. Taken together, we report a feedback loop of ANKHD1/MALAT1/YAP1 that synergistically promotes the transcriptional coactivation of YAP1 and in turn enhances the radioresistance of CRC by regulating DNA-damage repair, probably via the YAP1/AKT axis. Our results suggested that targeting the YAP1/AKT axis downstream of ANKHD1/MALAT1/YAP1 may enhance the radiosensitivity of CRC.

Indexed as

Cell Line, TumorColorectal NeoplasmsDNA Breaks, Double-StrandedDNA RepairFeedback, PhysiologicalGene Expression Regulation, NeoplasticHumansProto-Oncogene Proteins c-aktRadiation ToleranceRNA-Binding ProteinsRNA, Long NoncodingSignal TransductionYAP-Signaling ProteinsANKHD1 protein, humanMALAT1 long non-coding RNA, humanProto-Oncogene Proteins c-aktRNA-Binding ProteinsRNA, Long NoncodingYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID35110552
PMCPMC8810793
OpenAlexW4210645742

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.