Evidence map›Paper›PMID 41620562›Full record

ArticleCancer gene therapy2026

C1orf35 contributes to high anabolic metabolism by simultaneously promoting aerobic glycolysis and oxidative phosphorylation in multiple myeloma cells.

Rui He, Wei Xiong, Saiqun Luo, Ruoyan Dang, Xiang Zhou, Yan Wu, Wei-Xin Hu, Jingping Hu

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Article in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Review
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

8 authors.

Rui He *Molecular Biology Research Center, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha, China.
Wei Xiong *Molecular Biology Research Center, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha, China.
Saiqun LuoMolecular Biology Research Center, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha, China.
Ruoyan DangMolecular Biology Research Center, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha, China.
Xiang ZhouMolecular Biology Research Center, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha, China.
Yan WuDepartment of Metabolism & Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Wei-Xin HuMolecular Biology Research Center, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha, China.
Jingping HuMolecular Biology Research Center, School of Life Sciences; Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha, China. jingpinghu@csu.edu.cn.ORCID http://orcid.org/0000-0001-5548-1241

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82070229
6 · The paper itself

Abstract

Similar to other malignancies, multiple myeloma (MM) has acquired several functional capabilities known as "Hallmarks of cancer", and one of them is the deregulation of cell metabolism, especially glucose metabolism. Our current study focuses on the role of Chromosome 1 Open Reading Frame 35(C1orf35) in the glucose metabolism of MM cells. We found that the expression of C1orf35 was negative correlated with the overall survival of MM patients, MM cell lines with high C1orf35 expression not only had a faster proliferation rate but also higher levels of both aerobic glycolysis and oxidative phosphorylation (OXPHOS). Mechanistic studies revealed that C1orf35 promoted aerobic glycolysis through the c-MYC/PKM2 pathway and interacted with Leucine-Rich PPR Motif-Containing Protein (LRPPRC) to enhance OXPHOS. Moreover, treating MM cells with Gossypol Acetic Acid (GAA), a small molecule inhibitor specifically targeting LRPPRC, unexpectedly led to the degradation of C1orf35 protein and an "energy crisis" in these cells. Finally, we confirmed C1orf35 is on the upstream of PI3K/AKT/mTOR pathway, thus C1orf35 may play a pivotal role in anabolic metabolism. Our study uncovers a "C1orf35-driven" energy metabolism model in MM cells, providing new insights into the pathogenesis of MM and a potential novel target for the treatment of cancer cells with a high"C1orf35-driven" anabolic metabolism. Schematic diagram of C1orf35 simultaneously promotes glycolysis and OXPHOS.

Indexed as

GlycolysisMultiple MyelomaOxidative PhosphorylationAnimalsCell Line, TumorHumansMetabolic Reprogramming

Identifiers

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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.