Evidence map›Paper›PMID 33097691›Full record

ArticleCell death & disease2020

The miR-30a-5p/CLCF1 axis regulates sorafenib resistance and aerobic glycolysis in hepatocellular carcinoma.

Zhongqiang Zhang, Xiao Tan, Jing Luo, Hongliang Yao, Zhongzhou Si, Jing-Shan Tong

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

48 citing papers in PubMed, 84 citations in OpenAlex.

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  12. CLCF1 inhibits energy expenditure via suppressing brown fat thermogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Zhongqiang ZhangDepartment of Liver Transplantation, The Second Xiangya Hospital of Central South University, 410011, Changsha, Hunan Province, P.R. China.
Xiao TanDepartment of Oncology, Xiangya Hospital, Central South University, 410008, Changsha, Hunan Province, P.R. China.
Jing LuoDepartment of Liver Transplantation, The Second Xiangya Hospital of Central South University, 410011, Changsha, Hunan Province, P.R. China.
Hongliang YaoDepartment of General Surgery, The Second Xiangya Hospital of Central South University, 410011, Changsha, Hunan Province, P.R. China.ORCID 0000-0003-2447-8909
Zhongzhou SiDepartment of Liver Transplantation, The Second Xiangya Hospital of Central South University, 410011, Changsha, Hunan Province, P.R. China. zhongzsi@csu.edu.cn.
Jing-Shan TongDepartment of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213, USA. tongjingshan@gmail.com.
Central South University · CNUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HCC (hepatocellular carcinoma) is a major health threat for the Chinese population and has poor prognosis because of strong resistance to chemotherapy in patients. For instance, a considerable challenge for the treatment of HCC is sorafenib resistance. The aberrant glucose metabolism in cancer cells aerobic glycolysis is associated with resistance to chemotherapeutic agents. Drug-resistance cells and tumors were exposed to sorafenib to establish sorafenib-resistance cell lines and tumors. Western blotting and real-time PCR or IHC staining were used to analyze the level of CLCF1 in the sorafenib resistance cell lines or tumors. The aerobic glycolysis was analyzed by ECAR assay. The mechanism mediating the high expression of CLCF1 in sorafenib-resistant cells and its relationships with miR-130-5p was determined by bioinformatic analysis, dual luciferase reporter assays, real-time PCR, and western blotting. The in vivo effect was evaluated by xenografted with nude mice. The relation of CLCF1 and miR-30a-5p was determined in patients' samples. In this study, we report the relationship between sorafenib resistance and increased glycolysis in HCC cells. We also show the vital role of CLCF1 in promoting glycolysis by activating PI3K/AKT signaling and its downstream genes, thus participating in glycolysis in sorafenib-resistant HCC cells. Furthermore, we also show that miR-30a-5p directly targets CLCF1 and that sorafenib-mediated suppression of miR-30a-5p results in the upregulation of CLCF1 in HCC cells resistant to sorafenib. We also found that when a cholesterol modified agomiR-30a-5p was delivered systemically to mice harboring sorafenib-resistant HCC tumors, tumor growth decreased significantly. There is an uncharacterized mechanism of biochemical resistance to hormone therapies orchestrated by the miR-30a-5p/CLCF1 axis to mediate sorafenib resistance and aerobic glycolysis in HCC. Therefore, this study indicates that targeting the miR-30a-5p/CLCF1 axis may hold promise for therapeutic intervention in HCC sorafenib resistance patients.

Indexed as

SorafenibAnimalsAntineoplastic AgentsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceMicroRNAsSignal TransductionAntineoplastic AgentsMicroRNAsMIRN30a microRNA, mouseMIRN30b microRNA, humanSorafenib

Identifiers

PMID33097691
PMCPMC7584607
OpenAlexW3094346172

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.