Evidence map›Paper›PMID 40263288›Full record

ArticleCell death discovery2025

QKI-induced circ_0001766 inhibits colorectal cancer progression and rapamycin resistance by miR-1203/PPP1R3C/mTOR/Myc axis.

Yulai Zhou, Yan Gao, Yinghui Peng, Changjing Cai, Ying Han, Yihong Chen, Gongping Deng, Yanhong Ouyang, Hong Shen, Shan Zeng and 2 more

Abstract read
In one paragraph

Article in Cell death discovery, 2025. 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
–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

7 citing papers in PubMed.

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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.

Yulai Zhou *Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0002-1044-5148
Yan Gao *Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yinghui PengDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Changjing CaiDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ying HanDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yihong ChenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Gongping DengDepartment of Emergency, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan, China.
Yanhong OuyangDepartment of Emergency, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Hainan, China.
Hong ShenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Shan ZengDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yangfeng DuDepartment of Oncology, Changde Hospital, Xiangya School of Medicine, Central South University, Changde, Hunan, China. dyfer0924@163.com.ORCID http://orcid.org/0009-0009-8805-898X
Zemin XiaoDepartment of Oncology, Changde Hospital, Xiangya School of Medicine, Central South University, Changde, Hunan, China. xiaozemindoc@163.com.ORCID http://orcid.org/0009-0002-6445-7192

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third most common cancer and remains a significant challenge due to high rates of drug resistance and limited therapeutic options. Circular RNAs (circRNAs) are increasingly recognized for their roles in CRC initiation, progression, and drug resistance. However, no circRNA-based therapies have yet entered clinical development, underscoring the need for comprehensive detection and mechanistic studies of circRNAs in CRC. Here, we identified and characterized a circular RNA, circ_0001766 (hsa_circ_0001766), through microarray analysis of CRC tissues. Our results showed that circ_0001766 is downregulated in CRC tissues and closely associated with patient survival and metastasis. Functional experiments demonstrated that circ_0001766 inhibits CRC cell proliferation, migration and invasion both in-vitro and in-vivo. Mechanistically, hypoxia downregulates Quaking (QKI), an RNA-binding protein essential for the biogenesis of circ_0001766 by binding to introns 1 and 3 of PDIA4 pre-mRNA. Reduced QKI expression under hypoxic conditions leads to decreased circ_0001766 levels in CRC. Circ_0001766 acts as a competitive endogenous RNA, sponging miR-1203 to prevent the degradation of PPP1R3C mRNA. Loss of circ_0001766 results in decreased PPP1R3C expression, leading to the activation of mTOR signaling and increased phosphorylation of Myc, which promotes CRC progression and rapamycin resistance. Our study reveals that overexpression of circ_0001766 or PPP1R3C in CRC cells inhibits the mTOR and Myc pathway, thereby resensitizing cells to rapamycin. The combination of circ_0001766 or PPP1R3C with rapamycin markedly inhibits CRC cell proliferation and induces apoptosis by reducing rapamycin-induced Myc phosphorylation. In summary, our study elucidates a critical circ_0001766/miR-1203/PPP1R3C axis that modulates CRC progression and rapamycin resistance. Our findings highlight circ_0001766 as a promising therapeutic target in CRC, providing a new avenue for enhancing the efficacy of existing treatments and overcoming drug resistance.

Identifiers

PMID40263288
PMCPMC12015279

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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.