Evidence map›Paper›PMID 38981023›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

CircHIPK2 Contributes Cell Growth in Intestinal Epithelial of Colitis and Colorectal Cancer through Promoting TAZ Translation.

Xixi Zeng, Jielin Tang, Qian Zhang, Chenxing Wang, Ji Qi, Yusi Wei, Jiali Xu, Kaiyuan Yang, Zuolin Zhou, Hao Wu and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. CircPRKCA Promotes NSCLC Progression via miR-200b-3p/FRMD6/SNAI2 Axis.International journal of molecular sciences · 2026
    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

15 authors.

Xixi ZengKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Jielin TangChemical Biology Research Center at School of Pharmaceutical Sciences, Wenzhou Medical University, Zhejiang, 325035, China.
Qian ZhangKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Chenxing WangDepartment of Gastroenterology, The Second Affiliated Hospital and Yuying Children of Wenzhou Medical University, Zhejiang, 325003, China.
Ji QiKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Yusi WeiKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Jiali XuKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Kaiyuan YangKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Zuolin ZhouKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Hao WuKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Jiarong LuoKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Yi JiangDepartment of Gastroenterology, The Second Affiliated Hospital and Yuying Children of Wenzhou Medical University, Zhejiang, 325003, China.
Zengqiang SongChemical Biology Research Center at School of Pharmaceutical Sciences, Wenzhou Medical University, Zhejiang, 325035, China.
Jinyu WuKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.
Jianmin WuKey Laboratory of Laboratory Medicine, Ministry of Education, Institute of Genomic Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, 325035, China.ORCID 0000-0002-8223-1667

Funding

National Natural Sciences Foundation of China NSFC-81472651Wenzhou Science and Technology Foundation of China Y20210088Zhejiang Provincial Natural Sciences Foundation LY20H160016
6 · The paper itself

Abstract

Colorectal cancer (CRC) and inflammatory bowel disease (IBD) are escalating global health concerns. Despite their distinct clinical presentations, both disorders share intricate genetic and molecular interactions. The Hippo signaling pathway plays a crucial role in regulating cell processes and is implicated in the pathogenesis of IBD and CRC. Circular RNAs (circRNAs) have gained attention for their roles in various diseases, including IBD and CRC. However, a comprehensive understanding of specific circRNAs involved in both IBD and CRC, and their functional roles is lacking. Here, it is found that circHIPK2 (hsa_circRNA_104507) is a bona fide circRNA consistently upregulated in both IBD and CRC suggesting its potential as a biomarker. Furthermore, silencing of circHIPK2 suppressed the growth of CRC cells in vitro and in vivo. Interestingly, decreased circHipk2 potentiated dextran sulfate sodium (DSS)-induced colitis but alleviated colitis-associated tumorigenesis. Most significantly, mechanistic investigations further unveil that circHIPK2, mediated by FUS, interacting with EIF4A3 to promote the translation of TAZ, ultimately increasing the transcription of downstream target genes CCN1 and CCN2. Taken together, circHIPK2 emerges as a key player in the shared mechanisms of IBD and CRC, modulating the Hippo signaling pathway. CircHIPK2-EIF4A3 axis contributes to cell growth in intestinal epithelial of colitis and CRC by enhancing TAZ translation.

Indexed as

ColitisColorectal NeoplasmsProtein Serine-Threonine KinasesRNA, CircularTranscriptional Coactivator with PDZ-Binding Motif ProteinsAnimalsCell ProliferationDisease Models, AnimalHumansIntestinal MucosaMicePLK2 protein, humanProtein Serine-Threonine KinasesRNA, CircularTranscriptional Coactivator with PDZ-Binding Motif ProteinsWWTR1 protein, humancell growthcircHIPK2colorectal cancerinflammatory bowel diseaseTAZ

Identifiers

PMID38981023
PMCPMC11425914

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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.