Evidence map›Paper›PMID 36639711›Full record

ArticleCell death & disease2023

CircIFNGR2 enhances proliferation and migration of CRC and induces cetuximab resistance by indirectly targeting KRAS via sponging to MiR-30b.

Qi Zhang, Yifeng Zheng, Jiajia Liu, Xiaoxiao Tang, Yuan Wang, Xianzheng Li, Huibin Li, Xiaoying Zhou, Shiru Tang, Yitao Tang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 23 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

13 authors at 3 institutions in 1 country.

Qi Zhang *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yifeng Zheng *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Jiajia Liu *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xiaoxiao TangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yuan WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xianzheng LiMedical Genetic Center, Guangdong Women and Children Hospital, Guangzhou, Guangdong, China.
Huibin LiMedical Genetic Center, Guangdong Women and Children Hospital, Guangzhou, Guangdong, China.
Xiaoying ZhouDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Shiru TangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yitao TangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xiaoyan WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. wangxiaoyan639@163.com.ORCID 0000-0003-3009-8638
Han HeDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. 398069921@qq.com.
Tingting LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. 343730051@qq.com.ORCID 0000-0002-3207-0578
Guangzhou Experimental Station · CNGuangdong Province Women and Children Hospital · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently the clinical efficacy of colorectal cancer (CRC) which is the most common malignant tumors over the world has not reached an ideal level. Cetuximab, the monoclonal antibody targeting the extracellular domain of EGFR, has shown its great efficacy in the promotion of apoptosis and the inhibition of tumor cells-like characteristics in numerous cancers. However certain KRAS wild-type CRC patients unexpectedly show cetuximab resistance and the specific mechanism remains unclear. Circular RNAs (circRNAs) as the promising novel type of biomarkers in the cancer diagnosis and therapy, have been reported to be related with the drug resistance. In this study, with wondering the mechanism of cetuximab resistance in KRAS wild-type CRC patients, we evaluate the impact of circIFNGR2 on CRC and detect the association among circIFNGR2, miR-30b and KRAS via various experiments such as RT-qPCR, immunohistochemistry, luciferase assays, cell functional experiments and xenograft model. We conclude that circIFNGR2 induces cetuximab resistance in colorectal cancer cells by indirectly regulating target gene KRAS by sponging miR-30b at the post-transcriptional level. It is thus suggested that inhibition of circIFNGR2 can be a promising therapeutic strategy for malignant CRC patients with cetuximab resistance.

Indexed as

Colorectal NeoplasmsMicroRNAsProto-Oncogene Proteins p21(ras)RNA, CircularCell Line, TumorCell ProliferationCetuximabDrug Resistance, NeoplasmHumansMutationReceptors, InterferonCetuximabIFNGR2 protein, humanKRAS protein, humanMicroRNAsMIRN30b microRNA, humanProto-Oncogene Proteins p21(ras)Receptors, InterferonRNA, Circular

Identifiers

PMID36639711
PMCPMC9839739
OpenAlexW4315881068

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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.