Evidence map›Paper›PMID 35460941›Full record

ArticleTranslational oncology2022

Low doses of niclosamide and quinacrine combination yields synergistic effect in melanoma via activating autophagy-mediated p53-dependent apoptosis.

Xuan Zheng, Jianyun Zhang, Shuangting Li, Xiaolei Gao, Yixin Zhang, Meng Wang, Liying Dong, Liangjie Sun, Na Zhao, Zeyun Ma and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Translational oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Doramectin Induces Apoptosis in B16 Melanoma Cells.Anti-cancer agents in medicinal chemistry · 2025
    Article
  4. Article
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Xuan ZhengCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China; Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Jianyun ZhangDepartment of Oral Pathology, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Shuangting LiShanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Shanxi Medical University School and Hospital of Stomatology, Taiyuan 030001, China.
Xiaolei GaoCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China; Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Yixin ZhangCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China; Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Meng WangCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Liying DongCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China; Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Liangjie SunCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China; Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China.
Na ZhaoDepartment of Restorative Dentistry and Biomaterials Sciences, Harvard School of Dental Medicine, Boston, MA, USA; Shanghai Stomatological Hospital, Fudan University, No.356, Beijing Road East, Shanghai, China.
Zeyun MaDepartment of VIP Service, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China. Electronic address: kqmzy101@sina.com.
Chong DingCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China. Electronic address: idtbbsb@163.com.
Yixiang WangCentral Laboratory, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China; Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, No.22, Zhongguancun Avenue South, Haidian District, Beijing 100081, China. Electronic address: kqwangyx@bjmu.edu.cn.
King University · USPeking University · CNHarvard University · USShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma is a highly aggressive, malignant, and drug-resistant tumor. It lacks an efficient treatment approach. In this study, we developed a novel anti-melanoma strategy by using anti-tapeworm drug niclosamide and anti-malarial drug quinacrine, and investigated the molecular mechanism by in vitro and in vivo assays. Meanwhile, other types of tumor cells, immortalized epithelial cells and bone marrow mesenchymal stem cells were used to evaluate the universal role of anti-cancer and safety of the strategy. The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage. After inhibiting autophagy by Baf-A1, flow cytometry and western blot showed that the expression of apoptosis-related proteins was down-regulated and the number of apoptotic cells decreased. Subsequently, in the siRNA-mediated p53 knockdown cells, the expression of apoptosis-related proteins and the number of apoptotic cells were also reduced, while the expression of autophagy-related proteins including LC3B, p62 did not change significantly. To sum up, we developed a new, safe strategy for melanoma treatment by using low doses of niclosamide and quinacrine to treat melanoma; and found a novel mechanism by which the combination application of low doses of niclosamide and quinacrine exerts an efficient anti-melanoma effect through activation of autophagy-mediated p53-dependent apoptosis. The novel strategy was verified to exert a universal anti-cancer role in other types of cancer.

Indexed as

ApoptosisAutophagyMelanomaNiclosamideQuinacrine

Identifiers

PMID35460941
PMCPMC9048101
OpenAlexW4224296649

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.