Evidence map›Paper›PMID 33757557›Full record

ArticleInfectious agents and cancer2021

Hepatitis B virus induces sorafenib resistance in liver cancer via upregulation of cIAP2 expression.

Shouhua Zhang, Nuoya Li, Yanling Sheng, Wen Chen, Qiangliang Ma, Xin Yu, Jianping Lian, Junquan Zeng, Yipeng Yang, Jinlong Yan

Open access · goldAbstract read
In one paragraph

Article in Infectious agents and cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. WISP1 Inhibits Hepatocellular Carcinoma Cell Proliferation by Promoting CyclinD1 Ubiquitination and Downregulating its Expression.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
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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

10 authors at 6 institutions in 1 country.

Shouhua Zhang *Department of General Surgery, Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, Jiangxi, China.
Nuoya Li *Department of General Surgery, Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, Jiangxi, China.
Yanling ShengDepartment of Ultrasound, The Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang, China.
Wen ChenDepartment of Surgery, Jiangxi Provincial Cancer Hospital, Nanchang, China.
Qiangliang MaDepartment of dermatology, Ili Kazakh Autonomous State Chinese Medicine Hospital, Xinjiang, Uygur Autonomous Region, China.
Xin YuDepartment of General Surgery, Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, Jiangxi, China.
Jianping LianDepartment of Oncology, The Affiliated Hospital of Jinggangshan University, Ji'an, China.
Junquan ZengDepartment of Oncology, The Affiliated Hospital of Jinggangshan University, Ji'an, China.
Yipeng YangDepartment of General Surgery, Xinhua Hospital of Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Rd, Shanghai, China. yangyipeng@xinhuamed.com.cn.
Jinlong YanDepartment of General Surgery, Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, Jiangxi, China. yjl19880608@126.com.ORCID http://orcid.org/0000-0002-7040-0275
Nanchang University · CNJinggangshan University · CNAffiliated Hospital of Jiangxi University of Traditional Chinese Medicine · CNJiangxi Provincial Cancer Hospital · CNShanghai Jiao Tong University · CNXinjiang Uygur Autonomous Region Uygur Medicine Hospital · CN

Funding

National Natural Science Foundation of China 81360338National Natural Science Foundation of China 81960443The Foundation of Jiangxi Provincial Health Department 20195422
6 · The paper itself

Abstract

backgroundHBV promotes cell survival by upregulating the expression of the cellular inhibitor of apoptosis protein 2 (cIAP2), however whether it is involved in HBV-induced sorafenib resistance in liver cancer remains unclear.

methodscIAP2 overexpression and knockdown was adopted to assess the involvement of cIAP2 in HBV-induced sorafenib resistance. Anti-HBV drug lamivudine and Akt inhibitor were used to investigate the impact of HBV replication on cIAP2 expression and sorafenib resistance. Xenotransplantation mouse model was used to confirm the data on cell lines in vitro.

resultsLiver cancer cell line HepG2.215 showed increased cIAP2 expression and enhanced resistance to sorafenib. Upon sorafenib treatment, overexpression of cIAP2 in HepG2 lead to decreased cleaved caspase 3 level and increased cell viability, while knockdown of cIAP2 in HepG2.215 resulted in increased level of cleaved caspase 3 and decreased cell viability, suggesting the involvement of cIAP2 in HBV-induced sorafenib resistance. Furthermore, anti-HBV treatment reduced cIAP2 expression and partially restored sorafenib sensitivity in HepG2.215 cells. Xenotransplantation mouse model further confirmed that co-treatment with lamivudine and sorafenib could reduce sorafenib-resistant HepG2.215 tumor cell growth.

conclusioncIAP2 is involved in HBV-induced sorafenib resistance in liver cancer and anti-HBV treatments reduce cIAP2 expression and partially restore sorafenib sensibility.

Indexed as

cIAP2Hepatitis B virusLamivudineLiver cancerSorafenib resistance

Identifiers

PMID33757557
PMCPMC7988944
OpenAlexW3138710229

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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.