Evidence map›Paper›PMID 41094393›Full record

ArticleBiological procedures online2025

Rap2B-mediated reprogramming of the PI3K/AKT signaling axis drives resistance to cetuximab-targeted therapy in colorectal carcinoma.

Shanshan Zhang, Ying Wei, Tingting Liu, Chenhao Sun, Xiuzhen Ge, Yang Ni, Xiaonan Tang, Mridul Roy, Tingmin Chang, Xiaohong Kang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biological procedures online, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Shanshan Zhang *Department of Gastroenterology, The First Affiliated Hospital of Henan Medical University, No. 88 Jiankang Road, Xinxiang, Henan Province, 453100, China.
Ying Wei *Life Science Research Center, The First Affiliated Hospital of Henan Medical University, Xinxiang, Henan, China.
Tingting LiuLife Science Research Center, The First Affiliated Hospital of Henan Medical University, Xinxiang, Henan, China.
Chenhao SunDepartment of Gastroenterology, The First Affiliated Hospital of Henan Medical University, No. 88 Jiankang Road, Xinxiang, Henan Province, 453100, China.
Xiuzhen GeDepartment of Gastroenterology, The First Affiliated Hospital of Henan Medical University, No. 88 Jiankang Road, Xinxiang, Henan Province, 453100, China.
Yang NiDepartment of Radiation Oncology, The First Affiliated Hospital of Henan Medical University, No. 88 Jiankang Road, Xinxiang, Henan, 453100, China.
Xiaonan TangDepartment of Radiation Oncology, The First Affiliated Hospital of Henan Medical University, No. 88 Jiankang Road, Xinxiang, Henan, 453100, China.
Mridul RoyLife Science Research Center, The First Affiliated Hospital of Henan Medical University, Xinxiang, Henan, China.
Tingmin ChangDepartment of Gastroenterology, The First Affiliated Hospital of Henan Medical University, No. 88 Jiankang Road, Xinxiang, Henan Province, 453100, China. ctminmail@163.com.
Xiaohong KangDepartment of Radiation Oncology, The First Affiliated Hospital of Henan Medical University, No. 88 Jiankang Road, Xinxiang, Henan, 453100, China. kxhhgd@163.com.

Funding

Henan Health Commission Project 242102310117Henan Health Commission Project LHGJ20220969Henan Health Commission Project LHGJ20230504
6 · The paper itself

Abstract

backgroundTargeted therapy resistance represents a significant clinical challenge in cancer treatment. Rap2B, a member of the Ras superfamily of small GTPases, is frequently overexpressed in various cancers and has been implicated in promoting tumor progression and therapy resistance. However, the role and underlying mechanisms of Rap2B in cetuximab resistance in colorectal cancer (CRC) remain to be elucidated. This study aims to investigate Rap2B expression patterns in CRC models and explore the mechanisms by which Rap2B mediates cetuximab resistance.

resultsThe expression level of Rap2B in CRC cell lines exhibits a significant negative correlation with sensitivity to cetuximab. In vivo experiments demonstrated that Rap2B downregulation significantly reduced tumor growth and enhanced cetuximab efficacy. Knockdown of Rap2B increases cetuximab sensitivity by inhibiting the PI3K/AKT signaling pathway, resulting in reduced cell proliferation and enhanced apoptosis. Conversely, overexpression of Rap2B induces cetuximab resistance by activating the PI3K/AKT pathway.

conclusionThis study highlights a close association between Rap2B overexpression and cetuximab resistance in CRC. The enhanced expression of Rap2B plays a pivotal role in conferring resistance, by activating the PI3K/AKT signaling pathway. Targeting Rap2B or its downstream pathways has the potential to provide novel therapeutic strategies for overcoming cetuximab resistance in colorectal cancer.

Indexed as

Cetuximab resistanceColorectal cancerPI3K/AKT signaling pathwayRap2BTargeted therapy

Identifiers

PMID41094393
PMCPMC12522668

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.