Evidence map›Paper›PMID 35296779›Full record

ArticleActa pharmacologica Sinica2022

The small molecule chemical compound cinobufotalin attenuates resistance to DDP by inducing ENKUR expression to suppress MYH9-mediated c-Myc deubiquitination in lung adenocarcinoma.

Jia-Hao Liu, Hui-Ling Yang, Shu-Ting Deng, Zhe Hu, Wei-Feng Chen, Wei-Wei Yan, Ren-Tao Hou, Yong-Hao Li, Rui-Ting Xian, Ying-Ying Xie and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  14. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
  15. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
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

19 authors at 7 institutions in 1 country.

Jia-Hao Liu *Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Hui-Ling Yang *Cancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Shu-Ting DengCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Zhe HuCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Wei-Feng ChenCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Wei-Wei YanCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Ren-Tao HouCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Yong-Hao LiCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Rui-Ting XianCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Ying-Ying XieCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Yun SuKey Laboratory of Protein Modification and Degradation, Basic School of Guangzhou Medical University, Guangzhou, 511436, China.
Li-Yang WuKey Laboratory of Protein Modification and Degradation, Basic School of Guangzhou Medical University, Guangzhou, 511436, China.
Ping XuRespiratory Department, Peking University Shenzhen Hospital, Shenzhen, 518034, China.
Zhi-Bo ZhuCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Xiong LiuNanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yu-Ling DengDepartment of Chinese Medicine Rehabilitation, Pingxiang People's Hospital, Pingxiang, 337055, China.
Yu-Bing WangCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China. wangyubing95117@163.com.
Zhen LiuCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China. narcissus_jane@163.com.
Wei-Yi FangCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China. fangweiyi1975@163.com.
TCM-Intigrated Cancer Center of Southern Medical University · CNGuangzhou Medical University · CNSouthern Medical University · CNGuangdong Medical College · CNJiangxi Pingxiang People's Hospital · CNNanfang Hospital · CNPeking University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small molecule chemical compound cinobufotalin (CB) is reported to be a potential antitumour drug that increases cisplatin (DDP) sensitivity in nasopharyngeal carcinoma. In this study, we first found that CB decreased DDP resistance, migration and invasion in lung adenocarcinoma (LUAD). Mechanistic studies showed that CB induced ENKUR expression by suppressing PI3K/AKT signalling to downregulate c-Jun, a negative transcription factor of ENKUR. Furthermore, ENKUR was shown to function as a tumour suppressor by binding to β-catenin to decrease c-Jun expression, thus suppressing MYH9 transcription. Interestingly, MYH9 is a binding protein of ENKUR. The Enkurin domain of ENKUR binds to MYH9, and the Myosin_tail of MYH9 binds to ENKUR. Downregulation of MYH9 reduced the recruitment of the deubiquitinase USP7, leading to increased c-Myc ubiquitination and degradation, decreased c-Myc nuclear translocation, and inactivation of epithelial-mesenchymal transition (EMT) signalling, thus attenuating DDP resistance. Our data demonstrated that CB is a promising antitumour drug and may be a candidate chemotherapeutic drug for LUAD patients.

Indexed as

Adenocarcinoma of LungAntineoplastic AgentsCisplatinNasopharyngeal NeoplasmsAdaptor Proteins, Signal Transducingbeta CateninBufanolidesCalmodulin-Binding ProteinsCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansLung NeoplasmsMyosin Heavy ChainsMyosinsPhosphatidylinositol 3-KinasesAdaptor Proteins, Signal TransducingAntineoplastic Agentsbeta CateninBufanolidesCalmodulin-Binding ProteinscinobufotalinCisplatinENKUR protein, humanMYH9 protein, humanMyosin Heavy ChainsMyosinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTranscription FactorsUbiquitin-Specific Peptidase 7USP7 protein, humanchemoresistancecinobufotalinENKURlung adenocarcinomaMYH9

Identifiers

PMID35296779
PMCPMC9525298
OpenAlexW4221130604

What OpenQuestion holds

Textmetadata
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.