Evidence map›Paper›PMID 39472937›Full record

ArticleJournal of translational medicine2024

miR-1226-5p is involved in radioresistance of colorectal cancer by activating M2 macrophages through suppressing IRF1.

Jae Yeon Choi, Hyun Jeong Seok, Dong Hyeon Lee, Junhye Kwon, Ui Sup Shin, Incheol Shin, In Hwa Bae

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 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

7 authors.

Jae Yeon ChoiDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, 75 Nowon-Ro, Nowon-Gu, Seoul, 01812, Republic of Korea.
Hyun Jeong SeokDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, 75 Nowon-Ro, Nowon-Gu, Seoul, 01812, Republic of Korea.
Dong Hyeon LeeDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, 75 Nowon-Ro, Nowon-Gu, Seoul, 01812, Republic of Korea.
Junhye KwonMedical Sciences Substantiation Center, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
Ui Sup ShinDepartment of Surgery, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.
Incheol ShinDepartment of Life Science, Hanyang University, Seoul, Republic of Korea.
In Hwa BaeDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, 75 Nowon-Ro, Nowon-Gu, Seoul, 01812, Republic of Korea. ihbae@kirams.re.kr.ORCID 0000-0002-2826-349X

Funding

Ministry of Science and ICT, South Korea 50531-2024Ministry of Science and ICT, South Korea NRF-2017M2A2A7A01018542(50035-2019)Ministry of Science and ICT, South Korea NRF-2021R1A2C2005966(50698-2023)
6 · The paper itself

Abstract

backgroundAlthough the representative treatment for colorectal cancer (CRC) is radiotherapy, cancer cells survive due to inherent radioresistance or resistance acquired after radiation treatment, accelerating tumor malignancy and causing local recurrence and metastasis. However, the detailed mechanisms of malignancy induced after radiotherapy are not well understood. To develop more effective and improved radiotherapy and diagnostic methods, it is necessary to clearly identify the mechanisms of radioresistance and discover related biomarkers.

methodsTo analyze the expression pattern of miRNAs in radioresistant CRC, sequence analysis was performed in radioresistant HCT116 cells using Gene Expression Omnibus, and then miR-1226-5p, which had the highest expression in resistant cells compared to parental cells, was selected. To confirm the effect of miR-1226-5 on tumorigenicity, Western blot, qRT-PCR, transwell migration, and invasion assays were performed to confirm the expression of EMT factors, cell mobility and invasiveness. Additionally, the tumorigenic ability of miR-1226-5p was confirmed in organoids derived from colorectal cancer patients. In CRC cells, IRF1, a target gene of miR-1226-5p, and circSLC43A1, which acts as a sponge for miR-1226-5p, were discovered and the mechanism was analyzed by confirming the tumorigenic phenotype. To analyze the effect of tumor-derived miR-1226-5p on macrophages, the expression of M2 marker in co-cultured cells and CRC patient tissues were confirmed by qRT-PCR and immunohistochemical (IHC) staining analyses.

resultsThis study found that overexpressed miR-1226-5p in radioresistant CRC dramatically promoted epithelial-mesenchymal transition (EMT), migration, invasion, and tumor growth by suppressing the expression of its target gene, IRF1. Additionally, we discovered circSLC43A1, a factor that acts as a sponge for miR-1226-5p and suppresses its expression, and verified that EMT, migration, invasion, and tumor growth are suppressed by circSLC43A1 in radioresistant CRC cells. Resistant CRC cells-derived miR-1226-5p was transferred to macrophages and contributed to tumorigenicity by inducing M2 polarization and secretion of TGF-β.

conclusionsThis study showed that the circSLC43A1/miR-1226-5p/IRF1 axis is involved in radioresistance and cancer aggressiveness in CRC. It was suggested that the discovered signaling factors could be used as potential biomarkers for diagnosis and treatment of radioresistant CRC.

Indexed as

Cell MovementColorectal NeoplasmsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticInterferon Regulatory Factor-1MacrophagesMicroRNAsRadiation ToleranceAnimalsBase SequenceCarcinogenesisCell Line, TumorHCT116 CellsHumansMacrophage ActivationMiceInterferon Regulatory Factor-1IRF1 protein, humanMicroRNAscircSLC43A1IRF1M2 macrophagemiR-1226-5pRadioresistance of colorectal cancerTGF-βTumor malignancy

Identifiers

PMID39472937
PMCPMC11523791

What Socratic 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 Socratic graph.