Evidence map›Paper›PMID 36385558›Full record

ArticleExperimental & molecular medicine2022

Simultaneous treatment with sorafenib and glucose restriction inhibits hepatocellular carcinoma in vitro and in vivo by impairing SIAH1-mediated mitophagy.

Jing Zhou, Ji Feng, Yong Wu, Hui-Qi Dai, Guang-Zhi Zhu, Pan-Hong Chen, Li-Ming Wang, Guang Lu, Xi-Wen Liao, Pei-Zhi Lu and 6 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 35 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

16 authors at 2 institutions in 3 countries.

Jing Zhou *Department of Physiology, School of Basic Medical Sciences, Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Ji Feng *Department of Toxicology, School of Public Health, Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Yong Wu *Department of Toxicology, School of Public Health, Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Hui-Qi Dai *Department of Physiology, National University of Singapore, Singapore, 117593, Singapore.
Guang-Zhi Zhu *Department of Hepatobiliary Surgery, First Affiliated Hospital of Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Pan-Hong ChenDepartment of Physiology, School of Basic Medical Sciences, Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Li-Ming WangDepartment of Physiology, National University of Singapore, Singapore, 117593, Singapore.
Guang LuDepartment of Physiology, National University of Singapore, Singapore, 117593, Singapore.
Xi-Wen LiaoDepartment of Hepatobiliary Surgery, First Affiliated Hospital of Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Pei-Zhi LuDepartment of Toxicology, School of Public Health, Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Wen-Jing SuDepartment of Toxicology, School of Public Health, Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Shing Chuan HooiDepartment of Physiology, National University of Singapore, Singapore, 117593, Singapore.
Xin-Pin YeDepartment of Hepatobiliary Surgery, First Affiliated Hospital of Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China.
Han-Ming ShenDepartment of Physiology, National University of Singapore, Singapore, 117593, Singapore. hmshen@um.edu.mo.
Tao PengDepartment of Hepatobiliary Surgery, First Affiliated Hospital of Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China. p98720p@163.com.
Guo-Dong LuDepartment of Toxicology, School of Public Health, Guangxi Medical University, 530021, Nanning, Guangxi Province, P. R. China. golden_lu@hotmail.com.ORCID 0000-0001-6056-3196
Guangxi Medical University · CNNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transarterial chemoembolization (TACE) is the first-line treatment for unresectable intermediate-stage hepatocellular carcinoma (HCC). It is of high clinical significance to explore the synergistic effect of TACE with antiangiogenic inhibitors and the molecular mechanisms involved. This study determined that glucose, but not other analyzed nutrients, offered significant protection against cell death induced by sorafenib, as indicated by glucose deprivation sensitizing cells to sorafenib-induced cell death. Next, this synergistic effect was found to be specific to sorafenib, not to lenvatinib or the chemotherapeutic drugs cisplatin and doxorubicin. Mechanistically, sorafenib-induced mitophagy, as indicated by PINK1 accumulation, increased the phospho-poly-ubiquitination modification, accelerated mitochondrial membrane protein and mitochondrial DNA degradation, and increased the amount of mitochondrion-localized mKeima-Red engulfed by lysosomes. Among several E3 ubiquitin ligases tested, SIAH1 was found to be essential for inducing mitophagy; that is, SIAH1 silencing markedly repressed mitophagy and sensitized cells to sorafenib-induced death. Notably, the combined treatment of glucose restriction and sorafenib abolished ATP generation and mitophagy, which led to a high cell death rate. Oligomycin and antimycin, inhibitors of electron transport chain complexes, mimicked the synergistic effect of sorafenib with glucose restriction to promote cell death mediated via mitophagy inhibition. Finally, inhibition of the glucose transporter by canagliflozin (a clinically available drug used for type-II diabetes) effectively synergized with sorafenib to induce HCC cell death in vitro and to inhibit xenograft tumor growth in vivo. This study demonstrates that simultaneous treatment with sorafenib and glucose restriction is an effective approach to treat HCC, suggesting a promising combination strategy such as transarterial sorafenib-embolization (TASE) for the treatment of unresectable HCC.

Indexed as

Antineoplastic AgentsCarcinoma, HepatocellularChemoembolization, TherapeuticLiver NeoplasmsGlucoseHumansMitophagyNiacinamideSorafenibAntineoplastic AgentsGlucoseNiacinamideSorafenib

Identifiers

PMID36385558
PMCPMC9723179
OpenAlexW4309412966

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.