Evidence map›Paper›PMID 35091683›Full record

ArticleOncogene2022

CircVPS13C promotes pituitary adenoma growth by decreasing the stability of IFITM1 mRNA via interacting with RRBP1.

Weiyu Zhang, Siyu Chen, Qiu Du, Piaopiao Bian, Yutong Chen, Zexian Liu, Jian Zheng, Ke Sai, Yonggao Mou, Zhongping Chen and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Exosomal CircMFN2 Enhances the Progression of Pituitary Adenoma via the MiR-146a-3p/TRAF6/NF-κB Pathway.Journal of neurological surgery. Part A, Central European neurosurgery · 2025
    Article
  7. Article
  8. Review
  9. FTO-mediated DSP mMolecular cancer · 2024
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. 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

12 authors at 1 institution in 1 country.

Weiyu Zhang *Department of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Siyu Chen *Department of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Qiu Du *Department of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Piaopiao BianDepartment of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yutong ChenDepartment of Abdominal Oncology, cancer center of the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Zexian LiuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.ORCID http://orcid.org/0000-0001-9698-0610
Jian ZhengState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.ORCID http://orcid.org/0000-0001-9831-7038
Ke SaiDepartment of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yonggao MouDepartment of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Zhongping ChenDepartment of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.ORCID http://orcid.org/0000-0002-6226-5771
Xiang FanDepartment of Neurosurgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China. xiangfan@msn.com.ORCID http://orcid.org/0000-0001-8907-365X
Xiaobing JiangDepartment of Neurosurgery/Neuro-oncology, Sun Yat-sen University Cancer Center. State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China. jiangxiaob1@sysucc.org.cn.ORCID http://orcid.org/0000-0001-6566-7269
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CircRNAs play important roles in a variety of biological processes by acting as microRNA sponges and protein scaffolds or by encoding functional proteins. However, their functions and underlying mechanisms remain largely unknown. Distinctive circRNA patterns were explored by comparing nonfunctioning pituitary adenomas (NFPAs) and normal pituitary tissues with a circRNA array. The biological functions of selected circRNAs were determined in vitro and in vivo. RNA-seq and circRNA pulldown assays were applied to investigate the underlying mechanisms. The circRNA profile of NFPAs is tremendously different from that of normal pituitary tissues. CircVPS13C is significantly upregulated in NFPA samples and cell lines. Gain- and loss-of-function experiments demonstrate that silencing circVPS13C inhibits the proliferation of pituitary tumor cells in vitro and in vivo. Mechanistically, circVPS13C silencing increases the expression of IFITM1 and subsequently activates its downstream genes involved in MAPK- and apoptosis-associated signaling pathways. Rescue experiments show that IFITM1 overexpression partly reverses the biological effects of circVPS13C. Further studies reveal that circVPS13C inhibits IFITM1 expression through a novel mechanism mainly by competitively interacting with RRBP1, a ribosome-binding protein of the endoplasmic reticulum membrane, and thereby alleviating the stability of IFITM1 mRNA. Clinically, circVPS13C expression is markedly higher in high-risk NFPA samples and is downregulated in patient serum 7 days post-transsphenoidal adenoma resection. Our findings suggest that circVPS13C is a critical regulator in the proliferation and development of NFPAs through a novel mechanism, whereby regulating mRNA stability via interacting with ribosome-binding proteins on the endoplasmic reticulum membrane.

Indexed as

AdenomaBiological PhenomenaPituitary NeoplasmsHumansRNA, CircularRNA, MessengerRNA, CircularRNA, Messenger

Identifiers

PMID35091683
OpenAlexW4210388215

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.