Evidence map›Paper›PMID 37679975›Full record

ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2023

Active compounds of Caodoukou () inhibit the migration, invasion and metastasis of human pancreatic cancer cells by targeting phosphoinosmde-3-kinase/ protein kinase B/mammalian target of rapamycin pathway.

Yang Xiaohui, Wang Jian, Cheng Li, Zhang Yuxi, Huang Jianlin, Liu Minghua

Open access · greenAbstract read
In one paragraph

Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 72% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Journal of traditional and complementary medicine · 2026
    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

6 authors at 1 institution in 1 country.

Yang XiaohuiDepartment of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou 646000, China.
Wang JianDepartment of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou 646000, China.
Cheng LiDepartment of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou 646000, China.
Zhang YuxiDepartment of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou 646000, China.
Huang JianlinDepartment of Pharmacy, Luzhou Naxi District People's Hospital, Luzhou 646000, China.
Liu MinghuaDepartment of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou 646000, China.
Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo detect the effects of active compounds of Caodoukou () (ACAK) on the proliferation, migration and invasion of pancreatic cancer, and explain the possible molecular mechanism of ACAK interacting with these processes.

methodsCell counting kit-8 method, cell scratch repair experiment, Transwell migration and invasion experiment, immunohistochemistry, western blot assay and real-time polymerase chain reaction experiment were used to evaluate the effect of ACAK on the proliferation, migration and invasion of pancreatic cancer cells. The levels of active molecules involved in the phosphoinosmde-3-kinase (PI3K)/Akt/the mammalian target of rapamycin (mTOR) signal transduction were detected by Western blot assay. In addition, the function of ACAK was evaluated by xenotransplantation tumor model in nude mice.

resultsThe inhibitory effect of ACAK on the proliferation of pancreatic cancer cells showed certain time-dose dependence. The results of scratch repair test, Transwell test, Western blotting and real time polymerase chain reaction assay showed that ACAK could inhibit the migration and invasion of pancreatic cancer cells . In addition, the regulatory effect of ACAK on epithelial-mesenchymal transition (EMT) is partly attributed to PI3K/Akt/mTOR signaling pathway. The experimental results showed that ACAK regulated the development of pancreatic cancer.

conclusionsACAK can partly inhibit the activity of EMT and matrix metallopeptidases by down-regulating the downstream proteins of PI3K/Akt/mTOR signal pathway, thus inhibiting the ability of migration and invasion of pancreatic cancer.

Indexed as

Pancreatic NeoplasmsProto-Oncogene Proteins c-aktAnimalsDisease Models, AnimalHumansMammalsMiceMice, NudePhosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktactive compoundsCaodoukou ()migration and invasionpancreatic neoplasmsPI3KSignal transductionTOR serine-threonine kinases

Identifiers

PMID37679975
PMCPMC10465845
OpenAlexW4386530813

What OpenQuestion holds

Textmetadata
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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.