Evidence map›Paper›PMID 38760797›Full record

ArticleLipids in health and disease2024

Low expression of ELOVL6 may be involved in fat loss in white adipose tissue of cancer-associated cachexia.

Chenyang Jin, Shuangjie Wang, Xiangyu Sui, Qingyang Meng, Guohao Wu

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Article in Lipids in health and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

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5citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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5 citing papers in PubMed.

  1. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Chenyang Jin *Department of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China.
Shuangjie Wang *Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai, China.
Xiangyu SuiDepartment of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China.
Qingyang MengDepartment of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China. Leonmqy@126.com.
Guohao WuDepartment of General Surgery, Zhongshan Hospital of Fudan University, Shanghai, China. profwugh@163.com.

Funding

Shanghai Natural Science Foundation 19ZR1409100
6 · The paper itself

Abstract

backgroundCancer-associated cachexia (CAC) arises from malignant tumors and leads to a debilitating wasting syndrome. In the pathophysiology of CAC, the depletion of fat plays an important role. The mechanisms of CAC-induced fat loss include the enhancement of lipolysis, inhibition of lipogenesis, and browning of white adipose tissue (WAT). However, few lipid-metabolic enzymes have been reported to be involved in CAC. This study hypothesized that ELOVL6, a critical enzyme for the elongation of fatty acids, may be involved in fat loss in CAC.

methodsTranscriptome sequencing technology was used to identify CAC-related genes in the WAT of a CAC rodent model. Then, the expression level of ELOVL6 and the fatty acid composition were analyzed in a large clinical sample. Elovl6 was knocked down by siRNA in 3T3-L1 mouse preadipocytes to compare with wild-type 3T3-L1 cells treated with tumor cell conditioned medium.

resultsIn the WAT of patients with CAC, a significant decrease in the expression of ELOVL6 was found, which was linearly correlated with the extent of body mass reduction. Gas chromatographic analysis revealed an increase in palmitic acid (C16:0) and a decrease in linoleic acid (C18:2n-6) in these tissue samples. After treatment with tumor cell-conditioned medium, 3T3-L1 mouse preadipocytes showed a decrease in Elovl6 expression, and Elovl6-knockdown cells exhibited a reduction in preadipocyte differentiation and lipogenesis. Similarly, the knockdown of Elovl6 in 3T3-L1 cells resulted in a significant increase in palmitic acid (C16:0) and a marked decrease in oleic acid (C18:1n-9) content.

conclusionOverall, the expression of ELOVL6 was decreased in the WAT of CAC patients. Decreased expression of ELOVL6 might induce fat loss in CAC patients by potentially altering the fatty acid composition of adipocytes. These findings suggest that ELOVL6 may be used as a valuable biomarker for the early diagnosis of CAC and may hold promise as a target for future therapies.

Indexed as

3T3-L1 CellsAdipose Tissue, WhiteCachexiaFatty Acid ElongasesNeoplasmsAnimalsFatty AcidsFemaleHumansLipogenesisMaleMiceMiddle AgedPalmitic AcidELOVL6 protein, humanElovl6 protein, mouseFatty Acid ElongasesFatty AcidsPalmitic AcidCancer-associated cachexiaELOVL6Fat lossLong-chain fatty acid

Identifiers

PMID38760797
PMCPMC11100253

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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.