ArticleInternational journal of clinical oncology2026
Relationship between CCM3 expression and angiogenesis in esophageal squamous cell carcinoma and its possible mechanism.
Article in International journal of clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundAngiogenesis is essential for esophageal squamous cell carcinoma (ESCC) progression, yet clinically actionable regulators remain limited. We investigated the expression, functional role, and mechanism of CCM3 in ESCC and its relationship with the HIF-1α/VEGFA angiogenic axis.
methodsCCM3, HIF-1α, VEGFA and microvessel density (MVD, CD31) were assessed by immunohistochemistry in 53 paired ESCC and adjacent non-cancerous tissues. CCM3 knockdown was optimized using four siRNAs in KYSE-70 and KYSE270 cells. CCM3 siRNA 1064-A was selected as the most effective and optimal knockdown achieved at 8 nM, 48 h. Tumor-conditioned HUVECs (referred to as tumor-conditioned endothelial cells, TECs) were generated using conditioned media from knockdown cells; TEC proliferation (CCK8), migration (scratch), invasion (Transwell) and tube formation were evaluated in vitro. A subcutaneous xenograft model using KYSE-70 cells was employed in vivo, followed by intratumoral silencing of CCM3 to assess tumour development, proliferation (Ki-67), and microvessel density (CD31).
resultsHigh endogenous CCM3 expression was significantly upregulated in ESCC tissues compared to adjacent non-cancerous tissues and correlated with clinicopathological features like depth of invasion, lymph node metastasis and advanced stage. CCM3 expression positively correlated with HIF-1α and VEGFA. CCM3 knockdown siRNA 1064-A attenuates TEC proliferation, migration, invasion and tube formation in vitro. In vivo, CCM3 knockdown reduced tumor growth, tumor weight, Ki-67, CD31 staining and levels of HIF-1α and VEGFA.
conclusionsHigh endogenous CCM3 expression associates with aggressive ESCC clinicopathological features and angiogenesis markers. CCM3 knockdown inhibits tumor-conditioned endothelial function, xenograft growth, intratumoral vascularization, and HIF-1α/VEGFA expression, warranting further mechanistic investigation.
Indexed as
Identifiers
42417927What OpenQuestion holds
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.