RPL18 promotes melanoma progression and drug resistance via BTF3/STAT3-dependent mechanisms and immune modulation.

Chenchen Zuo, Chengjun Hu, Xulei Jiang, Xin Bu

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In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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.

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2 · The registry

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Chenchen ZuoDepartment of Plastic and Cosmetic Surgery, Xiangya Hospital, Central South University, No 87 Xiangya Road, Changsha, Hunan 410008, P.R. China.

Chengjun HuDepartment of Plastic and Cosmetic Surgery, Xiangya Hospital, Central South University, No 87 Xiangya Road, Changsha, Hunan 410008, P.R. China.

Xulei JiangDepartment of Plastic and Cosmetic Surgery, Xiangya Hospital, Central South University, No 87 Xiangya Road, Changsha, Hunan 410008, P.R. China.

Xin BuDepartment of Plastic and Cosmetic Surgery, Xiangya Hospital, Central South University, No 87 Xiangya Road, Changsha, Hunan 410008, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RPL18 has emerged as a regulator of tumor behavior beyond its canonical role in protein synthesis. Here, we show that RPL18 enhances melanoma progression and chemoresistance by engaging both intrinsic signaling and the tumor microenvironment. Using melanoma cell lines, patient-derived organoids, and xenograft models, we demonstrate that RPL18 stabilizes BTF3 mRNA, leading to increased BTF3 expression and activation of STAT3 signaling. This pathway promotes melanoma cell proliferation, migration, and resistance to temozolomide. In parallel, RPL18-driven STAT3 activation increases transforming growth factor β (TGF-β) secretion, which induces M2 macrophage polarization and fosters an immunosuppressive microenvironment. Pharmacologic inhibition of STAT3 suppresses RPL18-dependent oncogenic phenotypes and restores temozolomide sensitivity

Indexed as

cancerimmune responsemolecular interaction

Identifiers

PMID41550725

DOI10.1016/j.isci.2025.114469

PMCPMC12808902

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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.