Evidence map›Paper›PMID 33061432›Full record

ArticleOncoTargets and therapy2020

Saikosaponin D Inhibits Proliferation and Promotes Apoptosis Through Activation of MKK4-JNK Signaling Pathway in Pancreatic Cancer Cells.

Mengru Lai, Yuqing Ge, Meng Chen, Siya Sun, Jianzhen Chen, Rubin Cheng

Abstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021
    Review
  18. Article
  19. Article
  20. Tanshinone I inhibited growth of human chronic myeloid leukemia cells via JNK/ERK mediated apoptotic pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    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.

Mengru Lai *College of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou 310053, People's Republic of China.
Yuqing Ge *First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou 310006, People's Republic of China.
Meng ChenCollege of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou 310053, People's Republic of China.
Siya SunCollege of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou 310053, People's Republic of China.
Jianzhen ChenCollege of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou 310053, People's Republic of China.
Rubin ChengCollege of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou 310053, People's Republic of China.ORCID 0000-0003-3952-2730

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPancreatic cancer remains one of the most lethal malignancies and has few treatment options. Saikosaponin D (SSD), a major bioactive triterpene saponin isolated from

methodsHere, we investigated the effect of SSD on the proliferation and apoptosis of human pancreatic cancer BxPC3 and PANC1 cells and the mouse pancreatic cancer cell line Pan02. Cell viability was determined by MTT assays and cell apoptosis analyzed by DAPI staining and flow cytometry. Expression levels of apoptosis-regulating markers and activity of the MKK4-JNK signaling pathway were determined by Western blotting. The inhibitor SP600125 was applied to confirm the role of the JNK pathway in SSD efficiency.

resultsSSD significantly inhibited the proliferation of BxPC3, PANC1, and Pan02 cells in a concentration- and time-dependent manner. Flow-cytometry analysis indicated obvious apoptosis induction after SSD exposure. Furthermore, SSD significantly triggered cleavage of caspase 3 and caspase 9 proteins and increased the expression of FoxO3a. In addition, activity of the MKK4-JNK pathway was dramatically increased after treatment with SSD in BxPC3 cells. SSD obviously stimulated phosphorylation of JNK, cJun, and SEK1/MKK4 proteins within 30 minutes. The addition of SP600125 blocked the activation of SSD on the MKK4-JNK regulatory pathway and reversed the effects of SSD on proliferation inhibition and apoptosis induction in BxPC3 cells.

conclusionThese results revealed that SSD was capable of suppressing tumor growth and promoting apoptosis of pancreatic cancer cells via targeting the MKK4-JNK signaling pathway, indicating the possibility of further developing SSD as a potential therapeutic candidate for pancreatic cancer.

Indexed as

apoptosis inductionMKK4–JNK pathwaypancreatic cancerproliferation inhibitionsaikosaponin D

Identifiers

PMID33061432
PMCPMC7522527

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.