Evidence map›Paper›PMID 28327651›Full record

ArticleScientific reports2017

Inhibition of cathepsin S confers sensitivity to methyl protodioscin in oral cancer cells via activation of p38 MAPK/JNK signaling pathways.

Ming-Ju Hsieh, Chiao-Wen Lin, Mu-Kuan Chen, Su-Yu Chien, Yu-Sheng Lo, Yi-Ching Chuang, Yi-Ting Hsi, Chia-Chieh Lin, Jui-Chieh Chen, Shun-Fa Yang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Advances in Cathepsin S Inhibition: Challenges and Breakthroughs in Drug Development.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Bioactive small-molecule constituents of Lao plants.Journal of medicinal plant research · 2021
    Article
  13. Cathepsin S Evokes PARCancers · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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.

Ming-Ju HsiehCancer Research Center, Changhua Christian Hospital, Changhua, 500, Taiwan.
Chiao-Wen LinInstitute of Oral Sciences, Chung Shan Medical University, Taichung, 40201, Taiwan.
Mu-Kuan ChenDepartment of Otorhinolaryngology-Head and Neck Surgery, Changhua Christian Hospital, Changhua, 500, Taiwan.
Su-Yu ChienDepartment of Pharmacy, Changhua Christian Hospital, Changhua, 500, Taiwan.
Yu-Sheng LoCancer Research Center, Changhua Christian Hospital, Changhua, 500, Taiwan.
Yi-Ching ChuangCancer Research Center, Changhua Christian Hospital, Changhua, 500, Taiwan.
Yi-Ting HsiCancer Research Center, Changhua Christian Hospital, Changhua, 500, Taiwan.
Chia-Chieh LinCancer Research Center, Changhua Christian Hospital, Changhua, 500, Taiwan.
Jui-Chieh ChenDepartment of Biochemical Science and Technology, National Chiayi University, Chiayi, 600, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung, 40201, Taiwan.
Changhua Christian Hospital · TWChung Shan Medical University Hospital · TWChina Medical University · TWChung Shan Medical University · TWMingDao University · TWNational Chiayi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral cancer is one of the most common cancers in the world. Approximately 90% of oral cancers are subtyped to oral squamous cell carcinoma (OSCC). Despite advances in diagnostic techniques and improvement in treatment modalities, the prognosis remains poor. Therefore, an effective chemotherapy mechanism that enhances tumor sensitivity to chemotherapeutics is urgently needed. Methyl protodioscin (MP) is a furostanol bisglycoside with a wide range of beneficial effects, including anti-inflammatory and anti-cancer properties. The aim of the present study was to determine the antitumor activity of MP on OSCC and its underlying mechanisms. Our results show that treatment of OSCC cells with MP potently inhibited cell viability. Moreover, MP leading to cell cycle arrest at G2/M phase, which subsequently activates caspase-3, -8, -9 and PARP to induce cell apoptosis. Meanwhile, we also demonstrate that MP induces a robust autophagy in OSCC cells. The results indicate cathepsin S (CTSS) is involved in MP-induced apoptosis and autophagy by modulation of p38 MAPK and JNK1/2 pathways. These findings may provide rationale to combine MP with CTSS blockade for the effective treatment of OSCC.

Indexed as

MAP Kinase Signaling SystemApoptosisAutophagyCathepsinsCell Cycle CheckpointsCell DeathCell Line, TumorCell SurvivalDiosgeninHumansMouth NeoplasmsSaponinscathepsin SCathepsinsDiosgeninmethyl protodioscinSaponins

Identifiers

PMID28327651
PMCPMC5361207
OpenAlexW2600111905

What OpenQuestion 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 OpenQuestion graph.