Evidence map›Paper›PMID 38794215›Full record

ArticlePharmaceuticals (Basel, Switzerland)2024

HGFK1 Enhances the Anti-Tumor Effects of Angiogenesis Inhibitors via Inhibition of CD90+ CSCs in Hepatocellular Carcinoma.

Tao Li, Ling Liu, Li Li, Xiaoxuan Yao, Xiaoyuan Hu, Jiaxing Cheng, Zhenpu Chen, Jiyin Guo, Ruilei Li, Chunlei Ge and 2 more

Abstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2024. 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
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.

  1. 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

12 authors.

Tao LiCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.ORCID 0000-0001-5930-2757
Ling LiuCancer Institute, Xuzhou Medical University, Xuzhou 221002, China.
Li LiCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Xiaoxuan YaoCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Xiaoyuan HuCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Jiaxing ChengCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Zhenpu ChenCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Jiyin GuoCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Ruilei LiCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Chunlei GeCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Marie Chia-Mi LinCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.
Hong YaoCancer Biotherapy Center & Cancer Research Institute, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming 650106, China.

Funding

Prof. Guo Jun Expert Workstation in Yunnan Province 202105AF150038the Fundamental Research Project of Yunnan Provincial Department of Science and Technology 202301AT070129the Joint Special Funds for the Department of Science and Technology of Yunnan Province‑Kunming Medical University 202001AY070001-074the National Natural Science Foundation of China 82350117, 82160476, 32360046, 82260462, 82204314the Scientific Research Fund project of the YunNan Education Department 2023Y0655
6 · The paper itself

Abstract

The combination of anti-angiogenesis agents with immune-checkpoint inhibitors is a promising treatment for patients with advanced hepatocellular carcinoma (HCC); however, therapeutic resistance caused by cancer stem cells present in tumor microenvironments remains to be overcome. In this study, we report for the first time that the Kringle 1 domain of human hepatocyte growth-factor α chain (HGFK1), a previously described anti-angiogenesis peptide, repressed the sub-population of CD90+ cancer stem cells (CSCs) and promoted their differentiation and chemotherapy sensitivity mainly through downregulation of pre-Met protein expression and inhibition of Wnt/β-catenin and Notch pathways. Furthermore, we showed that the i.p. injection of PH1 (a tumor-targeted and biodegradable co-polymer), medicated plasmids encoding Endostatin (pEndo), HGFK1 genes (pEndo), and a combination of 50% pEndo + 50% pHGFK1 all significantly suppressed tumor growth and prolonged the survival of the HCC-bearing mice. Importantly, the combined treatment produced a potent synergistic effect, with 25% of the mice showing the complete clearance of the tumor via a reduction in the microvessel density (MVD) and the number of CD90+ CSCs in the tumor tissues. These results suggest for the first time that HGFK1 inhibits the CSCs of HCC. Furthermore, the combination of two broad-spectrum anti-angiogenic factors, Endo and HGFK1, is the optimal strategy for the development of effective anti-HCC drugs.

Indexed as

CD90+ cancer stem cells (CSCs)chemotherapy drug cisplatin (CDDP)hepatocellular carcinoma (HCC)HGFK1nanoparticles

Identifiers

PMID38794215
PMCPMC11125149

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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.