Evidence map›Paper›PMID 30402948›Full record

ArticleCancer medicine2018

Purified vitexin compound 1, a new neolignan isolated compound, promotes PUMA-dependent apoptosis in colorectal cancer.

Jingfei Chen, Juchang Zhong, Yeying Liu, Yuan Huang, Fei Luo, Yingjun Zhou, Xi Pan, Shousong Cao, Lingling Zhang, Yingjie Zhang and 1 more

Abstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer Functions.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Natural Products as Modulators of Sirtuins.Molecules (Basel, Switzerland) · 2020
    Review
  9. Review
  10. Article
  11. 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

11 authors.

Jingfei ChenDepartment of Internal Medicine, The Third Xiangya Hospital, Central South University, Changsha, China.
Juchang ZhongCollege of Biology, Hunan University, Changsha, China.
Yeying LiuDepartment of Internal Medicine, The Third Xiangya Hospital, Central South University, Changsha, China.
Yuan HuangCollege of Biology, Hunan University, Changsha, China.
Fei LuoDepartment of Cardiology, The Second Xiangya Hospital, Changsha, China.
Yingjun ZhouSchool of Pharmaceutical Science, Central South University, Changsha, China.
Xi PanDepartment of Oncology, The Third Xiangya Hospital, Central South University, Changsha, China.
Shousong CaoDepartment of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou, China.ORCID 0000-0001-6892-0143
Lingling ZhangDepartment of Laboratory Medicine, Xiangya School of Medicine, Central South University, Changsha, China.
Yingjie ZhangCollege of Biology, Hunan University, Changsha, China.ORCID 0000-0001-9981-9523
Jiangang WangDepartment of Internal Medicine, The Third Xiangya Hospital, Central South University, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purified vitexin compound 1 (VB1, a neolignan isolated and extracted from the seed of Chinese herb Vitex negundo) is an effective antitumor agent and exhibits promising clinical activity against various cancers including colorectal cancer. However, it remains unknown about the precise underlying mechanism associated with the antitumor effect of VB1 and how it triggers apoptosis in cancer cells. Here, we demonstrated that VB1 promoted apoptosis via p53-dependent induction of p53 upregulated modulator of apoptosis (PUMA) and further to induce Bax (Bcl-2-associated X protein) activation and mitochondrial dysfunction in colon cancer HCT-116 and LoVo cells. Deficiency in p53, PUMA, or Bax abrogated VB1-induced apoptosis and promoted cell survival in HCT-116 cells. Furthermore, the combination of VB1 with chemotherapeutic drugs 5-fluorouracil (5-FU) or NVP-BZE235 resulted in a synergistic antitumor effect via PUMA induction in HCT-116 cells. VB1 significantly suppressed the cell proliferation of wild-type (WT) HCT-116 and LoVo cells in vitro and tumor growth in vivo. The results indicate that p53/PUMA/Bax axis plays a critical role in VB1-induced apoptosis and VB1 may have valuable clinical applications in cancer therapy as a novel anticancer agent used alone or in combination with other chemotherapeutic drugs.

Indexed as

AnimalsAntineoplastic AgentsApigeninApoptosisApoptosis Regulatory Proteinsbcl-2-Associated X ProteinCell Line, TumorCell ProliferationColorectal NeoplasmsFemaleHumansMice, NudeProto-Oncogene ProteinsTumor Suppressor Protein p53Antineoplastic AgentsApigeninApoptosis Regulatory ProteinsBBC3 protein, humanbcl-2-Associated X ProteinProto-Oncogene ProteinsTumor Suppressor Protein p53vitexinapoptosisBcl-2-associated X proteincolorectal cancerp53PUMAvitexin compound 1

Identifiers

PMID30402948
PMCPMC6308053

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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.