Evidence map›Paper›PMID 28356979›Full record

ArticleOncology letters2017

Inhibition of store-operated Ca

Wei Huang, Caiping Ren, Guoling Huang, Jie Liu, Weidong Liu, Lei Wang, Bin Zhu, Xiangling Feng, Jia Shi, Jinlong Li and 5 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. l-ornithine activates CaCellular signalling · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. 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

15 authors at 2 institutions in 1 country.

Wei HuangKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China; Research Center of Carcinogenesis and Targeted Therapy, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Caiping RenKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Guoling HuangKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Jie LiuKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Weidong LiuKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Lei WangKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Bin ZhuKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Xiangling FengKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Jia ShiKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Jinlong LiKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Xiaomeng XiaDepartment of Gynecology and Obstetrics, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Wei JiaKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Jiawen ChenKey Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China; Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University, Changsha, Hunan 410008, P.R. China.
Yuxiang ChenSchool of Pharmaceutical Sciences, Central South University, Changsha, Hunan 410008, P.R. China.
Xingjun JiangDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sodium butyrate (NaBu), a histone deacetylase inhibitor, has demonstrated anti-tumor effects in several cancers, and is a promising candidate chemotherapeutic agent. However, its roles in nasopharyngeal carcinoma (NPC), an endemic malignant disease in Southern China and Southeast Asia, has rarely been studied. In the present study, MTT assay, colony formation assay, flow cytometry analysis and western blotting were performed to explore the influence of NaBu on NPC cells and its underlying mechanism. NaBu induced morphological changes and inhibited proliferation in 5-8F and 6-10B cells. MTT assay revealed that NaBu was cytotoxic to 5-8F and 6-10B cells in a dose- and time-dependent manner. Furthermore, flow cytometry analysis revealed that NaBu induced obvious cell apoptosis in 5-8F and 6-10B cells due to the activation of the mitochondrial apoptosis axis. In addition, flow cytometry analysis and western blotting demonstrated that NaBu could enhance the Ca

Indexed as

mitochondrial apoptosisnasopharyngeal carcinomaSOCEsodium butyrate

Identifiers

PMID28356979
PMCPMC5351044
OpenAlexW2560578620

What OpenQuestion holds

Textmetadata
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.