Evidence map›Paper›PMID 37729394›Full record

ArticleCancer research2023

Fatty Acid Oxidation Mediated by Malonyl-CoA Decarboxylase Represses Renal Cell Carcinoma Progression.

Lijie Zhou, Yongbo Luo, Yuenan Liu, Youmiao Zeng, Junwei Tong, Mengting Li, Yaxin Hou, Kaixuan Du, Yabin Qi, Wenbang Pan and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
17.0field-weighted citation impact, top 1% of its field
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

40 citing papers in PubMed, 65 citations in OpenAlex.

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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

15 authors at 6 institutions in 1 country.

Lijie Zhou *Department of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0000-0002-2425-6946
Yongbo Luo *Department of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0009-0004-5627-9650
Yuenan Liu *Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.ORCID 0000-0002-4635-0634
Youmiao ZengDepartment of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0009-0001-2902-6533
Junwei TongDepartment of Urology, Traditional Chinese and Western Medicine Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0009-0005-2742-1838
Mengting LiDepartment of Nuclear Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0002-0715-0015
Yaxin HouDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.ORCID 0009-0005-6070-3589
Kaixuan DuDepartment of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0009-0000-2541-2683
Yabin QiDepartment of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0009-0007-5430-2628
Wenbang PanDepartment of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0009-0004-4413-776X
Yuanhao LiuDepartment of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0009-0001-9689-8622
Rongli WangDepartment of Obstetrics and Gynecology, First Affiliated Hospital, Xi'an Jiao tong University, Xi'an, China.ORCID 0000-0002-9877-3794
Fengyan TianDepartment of Pediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0002-7360-1582
Chaohui GuDepartment of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0000-0002-1552-948X
Ke ChenDepartment of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.ORCID 0000-0002-2098-1921
First Affiliated Hospital of Zhengzhou University · CNWuhan Union Hospital · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNKey Laboratory of Guangdong Province · CNTongji Hospital · CNWuhan No.1 Hospital · CN

Funding

Funding for Scientific Research and Innovation Team of The First Affiliated Hospital of Zhengzhou University NO.QNCXTD2023023National Natural Science Foundation of China (NSFC) NO. 82103000National Natural Science Foundation of China (NSFC) NO. 82173294National Natural Science Foundation of China (NSFC) NO. 82203099the Joint Construction Project between Medical Science and Technology Research Project of Henan Province NO. LHGJ20220335Training Program for Middle-aged and Young Discipline Leaders of Health of Henan Province NO. HNSWJW-2021004
6 · The paper itself

Abstract

Fatty acid metabolism reprogramming is a prominent feature of clear cell renal cell carcinoma (ccRCC). Increased lipid storage supports ccRCC progression, highlighting the importance of understanding the molecular mechanisms driving altered fatty acid synthesis in tumors. Here, we identified that malonyl-CoA decarboxylase (MLYCD), a key regulator of fatty acid anabolism, was downregulated in ccRCC, and low expression correlated with poor prognosis in patients. Restoring MLYCD expression in ccRCC cells decreased the content of malonyl CoA, which blocked de novo fatty acid synthesis and promoted fatty acid translocation into mitochondria for oxidation. Inhibition of lipid droplet accumulation induced by MLYCD-mediated fatty acid oxidation disrupted endoplasmic reticulum and mitochondrial homeostasis, increased reactive oxygen species levels, and induced ferroptosis. Moreover, overexpressing MLYCD reduced tumor growth and reversed resistance to sunitinib in vitro and in vivo. Mechanistically, HIF2α inhibited MLYCD translation by upregulating expression of eIF4G3 microexons. Together, this study demonstrates that fatty acid catabolism mediated by MLYCD disrupts lipid homeostasis to repress ccRCC progression. Activating MLYCD-mediated fatty acid metabolism could be a promising therapeutic strategy for treating ccRCC. SIGNIFICANCE: MLYCD deficiency facilitates fatty acid synthesis and lipid droplet accumulation to drive progression of renal cell carcinoma, indicating inducing MYLCD as a potential approach to reprogram fatty acid metabolism in kidney cancer.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsCarboxy-LyasesFatty AcidsHumansLipid MetabolismCarboxy-LyasesFatty Acidsmalonyl-CoA decarboxylase

Identifiers

PMID37729394
PMCPMC10690093
OpenAlexW4386883271

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.