ArticleGenetics research2022
OPN Promotes Cell Proliferation and Invasion through NF-
Article in Genetics research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Targeting the Osteopontin-regulated PI3K/AKT signaling pathway: A molecular approach to overcome drug resistance and metastasis in gastrointestinal tumors.World journal of gastrointestinal oncology · 2025Review
- Role of osteopontin in cancer: From pathogenesis to therapeutics (Review).Oncology reports · 2025Review
- Biological implications of decoding the extracellular matrix of vulva cancer.Oncology reports · 2025Review
- Osteopontin and Clinical Outcomes in Hemodialysis Patients.Biomedicines · 2024Article
- A new prognostic model of esophageal squamous cell carcinoma based on Cloud-least squares support vector machine.Journal of thoracic disease · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Osteopontin (OPN) is a phosphorylated glycoprotein. There is increasing evidence that the OPN gene played a major role in the progression of solid organ tumors. However, few studies have clarified how OPN regulated the functional role of human esophageal squamous cell carcinoma (ESCC). This study was designed to investigate the effect of OPN in esophageal squamous cell carcinoma. Methods: First, we screened Eca-109 and KYSE-510 cells to construct OPN silencing and overexpression models. Endogenous OPN of Eca-109 and KYSE-510 were knocked down or overexpressed using small interfering RNAs. QRT-PCR, Western blot, flow cytometry, and CCK-8 were used to detect the function of Eca-109 and KYSE-510 cells. Tumor formation in nude mice was used to measure tumor growth after OPN inhibition. Results: Eca-109 and KYSE-510 cells contain the si-OPN arrest cell cycle in the S-phase and increase apoptosis. These changes were OPN downregulation of the NF- Conclusion: This study contributed to understanding the vital role of OPN in ESCC development and progression. This could be a promising molecular target for developing new ESCC diagnostic and therapeutic strategies.
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Registered trials
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.