Evidence map›Paper›PMID 30253740›Full record

ArticleBMC cell biology2018

Tanshinone IIA reduces SW837 colorectal cancer cell viability via the promotion of mitochondrial fission by activating JNK-Mff signaling pathways.

Sayilaxi Jieensinue, Hong Zhu, Guangcheng Li, Keli Dong, Meiting Liang, Yayue Li

Open access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  11. Frontiers in immunology · 2024
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  13. Review
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  15. Article
  16. Article
  17. Tanshinone IIA May Inhibit Gastric Cancer via Affecting the Intestinal Microbiome.Computational and mathematical methods in medicine · 2022
    Article
  18. Article
  19. Frontiers in pharmacology · 2022
    Review
  20. Article
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

6 authors at 2 institutions in 1 country.

Sayilaxi JieensinueDepartment of Traditional Chinese Medicine, Central South University Third Xiangya Hospital, Changsha, 410013, China.
Hong ZhuDepartment of Traditional Chinese Medicine, Central South University Third Xiangya Hospital, Changsha, 410013, China. hongzhu3651@hotmail.com.
Guangcheng LiDepartment of Traditional Chinese Medicine, Central South University Third Xiangya Hospital, Changsha, 410013, China.
Keli DongDepartment of Traditional Chinese Medicine, Central South University Third Xiangya Hospital, Changsha, 410013, China.
Meiting LiangDepartment of Traditional Chinese Medicine, Central South University Third Xiangya Hospital, Changsha, 410013, China.
Yayue LiDepartment of Traditional Chinese Medicine, Central South University Third Xiangya Hospital, Changsha, 410013, China.
Central South University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondrial homeostasis has been increasingly viewed as a potential target of cancer therapy, and mitochondrial fission is a novel regulator of mitochondrial function and apoptosis. The aim of our study was to determine the detailed role of mitochondrial fission in SW837 colorectal cancer cell viability, mobility and proliferation. In addition, the current study also investigated the therapeutic impact of Tanshinone IIA (Tan IIA), a type of anticancer adjuvant drug, on cancer mitochondrial homeostasis.

resultsThe results of our data illustrated that Tan IIA promoted SW837 cell death, impaired cell migration and mediated cancer proliferation arrest in a dose-dependent manner. Functional investigation exhibited that Tan IIA treatment evoked mitochondrial injury, as witnessed by mitochondrial ROS overproduction, mitochondrial potential collapse, antioxidant factor downregulation, mitochondrial pro-apoptotic protein upregulation, and caspase-9-dependent apoptotic pathway activation. Furthermore, we confirmed that Tan IIA mediated mitochondrial damage by activating mitochondrial fission, and the inhibition of mitochondrial fission abrogated the proapoptotic effects of Tan IIA on SW837 cells. To this end, our results demonstrated that Tan IIA modulated mitochondrial fission via the JNK-Mff pathways. The blockade of the JNK-Mff axis inhibited Tan IIA-mediated mitochondrial fission and promoted the survival of SW837 cells.

conclusionsAltogether, our results identified mitochondrial fission as a new potential target to control cancer viability, mobility and proliferation. Furthermore, our findings demonstrate that Tan IIA is an effective drug to treat colorectal cancer by activating JNK-Mff-mitochondrial fission pathways.

Indexed as

AbietanesApoptosisCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationCell SurvivalColorectal NeoplasmsHumansMAP Kinase Signaling SystemMembrane ProteinsMitochondriaMitochondrial DynamicsMitochondrial ProteinsAbietanesMembrane ProteinsMff protein, humanMitochondrial ProteinstanshinoneColorectal cancerJNK-Mff pathwaysMitochondrial fissionMitochondrial injuryTanshinone IIA

Identifiers

PMID30253740
PMCPMC6157045
OpenAlexW2892548826

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.