Evidence map›Paper›PMID 29243194›Full record

ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2018

Kallistatin inhibits lymphangiogenesis and lymphatic metastasis of gastric cancer by downregulating VEGF-C expression and secretion.

Caiqi Ma, Chuanghua Luo, Haofan Yin, Yang Zhang, Wenjun Xiong, Ting Zhang, Tianxiao Gao, Xi Wang, Di Che, Zhenzhen Fang and 12 more

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In one paragraph

Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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  10. Lymphangiogenesis in gastric cancer: function and mechanism.European journal of medical research · 2023
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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

22 authors at 5 institutions in 2 countries.

Caiqi MaProgram of Molecular Medicine, Affiliated Guangzhou Women and Children's Hospital, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Chuanghua LuoProgram of Molecular Medicine, Affiliated Guangzhou Women and Children's Hospital, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Haofan YinDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Yang ZhangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Wenjun XiongDepartment of Gastrointestinal Surgery, Traditional Chinese Medicine Hospital of Guangdong Province, Guangzhou, China.
Ting ZhangDepartment of Clinical Laboratory, Guangzhou First People's Hospital, Guangzhou, China.
Tianxiao GaoDepartment of Hematologic Oncology, Sun Yat-sen University Cancer Center, Guangzhou, 510080, China.
Xi WangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Di CheProgram of Molecular Medicine, Affiliated Guangzhou Women and Children's Hospital, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Zhenzhen FangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Lei LiReproductive Medicine Center, the Third Hospital Affiliated to Guangzhou Medical University, Guangzhou, China.
Jinye XieDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Mao HuangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Liuqing ZhuDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Ping JiangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Weiwei QiDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Ti ZhouDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Zhonghan YangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Wei WangDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Jianxing MaDepartment of Physiology, University of Oklahoma, Health Sciences Center, Oklahoma City, OK, 73104, USA.
Guoquan GaoProgram of Molecular Medicine, Affiliated Guangzhou Women and Children's Hospital, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China. gaogq@mail.sysu.edu.cn.
Xia YangProgram of Molecular Medicine, Affiliated Guangzhou Women and Children's Hospital, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China. yangxia@mail.sysu.edu.cn.
Sun Yat-sen University · CNGuangzhou Medical University · CNGuangdong Provincial Hospital of Traditional Chinese Medicine · CNSun Yat-sen University Cancer Center · CNUniversity of Oklahoma Health Sciences Center · US

Funding

National Nature Science Foundation of China 81272338National Nature Science Foundation of China 81272515
6 · The paper itself

Abstract

backgroundTumor-induced lymphangiogenesis and lymphatic metastasis are predominant during the metastasis of many types of cancers. However, the endogenous inhibitors that counterbalance the lymphangiogenesis and lymphatic metastasis of tumors have not been well evaluated. Kallistatin has been recognized as an endogenous angiogenesis inhibitor. METHODS AND

resultsOur recent study showed for the first time that the lymphatic vessel density (LVD) was reduced in lung and stomach sections from kallistatin-overexpressing transgenic mice. Kallistatin expresses anti-lymphangiogenic activity by inhibiting the proliferation, migration, and tube formation of human lymphatic endothelial cells (hLECs). Therefore, the present study focuses on the relationships of changes in kallistatin expression with the lymphangiogenesis and lymphatic metastasis of gastric cancer and its underlying mechanisms. Our results revealed that the expression of kallistatin in cancer tissues, metastatic lymph nodes, and plasma of gastric cancer patients was significantly downregulated and that the plasma level of kallistatin was negatively associated with the phase of lymph node metastasis. Furthermore, treatment with kallistatin recombinant protein decreased LVD and lymph node metastases in the implanted gastric xenograft tumors of nude mice. Mechanically, kallistatin suppressed the lymphangiogenesis and lymphatic metastasis by downregulating VEGF-C expression and secretion through the LRP6/IKK/IҡB/NF-ҡB signaling pathway in gastric cancer cells.

conclusionsThese findings demonstrated that kallistatin functions as an endogenous lymphangiogenesis inhibitor and has an important part in the lymphatic metastasis of gastric cancer.

Indexed as

AgedAnimalsCell Line, TumorDown-RegulationFemaleHumansLow Density Lipoprotein Receptor-Related Protein-6LymphangiogenesisLymphatic MetastasisMaleMice, Inbred BALB CMiddle AgedRecombinant ProteinsSerpinsStomach NeoplasmsVascular Endothelial Growth Factor CkallistatinLow Density Lipoprotein Receptor-Related Protein-6LRP6 protein, humanRecombinant ProteinsSerpinsVascular Endothelial Growth Factor CGastric cancerKallistatinLRP6LymphangiogenesisLymph node metastasisNF-ҡBVEGF-C

Identifiers

PMID29243194
OpenAlexW2772160241

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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.