ArticleInternational journal of oncology2025
Targeting CALR reduces energy metabolism of esophageal cancer cells and inhibits tumor‑associated fibroblast infiltration.
Article in International journal of oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Lactylation-augmented DCBLD1-mediated PDIA3 stabilization reprograms glycolysis metabolism in oesophageal cancer.Journal of cancer research and clinical oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calreticulin (CALR) supports the induction of dendritic cell maturation, which makes it a key target for effective esophageal squamous cell carcinoma (ESCC) immunotherapy. The mechanism of CALR in the immunotherapy of ESCC is not fully studied. The aim of the present study was to explore the contributing role of CALR in ESCC progression. The association of CALR expression with calnexin (CANX) and protein disulfide isomerase A3 (PDIA3) expression in ESCC was analyzed. The functions of CALR in ESCC cells were examined by detection of cell migration, endoplasmic reticulum (ER) stress, mitochondrial function, cytoskeletal remodeling, cell proliferation and apoptosis. The effects of CALR on tumor growth and tumor‑associated fibroblast infiltration were examined by subcutaneous xenograft assay. The expression of CALR, CANX and PDIA3 in ESCC tissue significantly increased and the expression of PDIA3 was positively associated with CANX. Overexpression of CALR resulted in enhanced cell proliferation, migration, ER stress, mitochondrial function and cytoskeletal remodeling; knockdown of CALR expression had the opposite effect. In the subcutaneous xenograft assay, knockdown CALR significantly inhibited the growth of esophageal cancer tumors, suppressed the invasion of tumor‑associated fibroblasts and decreased the expression of α‑smooth muscle actin (α‑SMA), fibroblast activation protein (FAP), fibroblast specific protein‑1 (FSP1), platelet‑derived growth factor and transforming growth factor beta (TGF‑β) in tumor tissue. These findings suggested that CALR promotes the progression of ESCC by regulating ER stress and mitochondrial function to mediate ATP production, cytoskeletal remodeling, cell proliferation and apoptosis through CANX and PDIA3. Knockdown CALR significantly inhibited tumor‑associated fibroblast infiltration and is a potential drug target for ESCC.
Indexed as
Identifiers
What 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.