ReviewCancer gene therapy2026
SPARC family proteins: matricellular modulators of cancer progression and therapeutic resistance.
Review in Cancer gene therapy, 2026. 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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The SPARC (secreted protein acidic and rich in cysteine) family represents a unique class of matricellular proteins - including SPARC, SPARCL1, SPOCK1-3, SMOC1-2, and FSTL1 - that regulate extracellular matrix (ECM) dynamics, cell signaling, and tissue homoeostasis. In cancer, their expression is frequently dysregulated, through epigenetic mechanisms, microRNAs, and interactions within the tumor microenvironment (TME). Dysregulation of SPARC family members is most pronounced in aggressive malignancies with SPARC, SPARCL1, SPOCK1, and SPOCK2 most consistently altered. These proteins drive tumor progression through ECM remodeling, epithelial-mesenchymal transition (EMT), maintenance of cancer stemness, immune modulation, and drug resistance acquisition. Their functions are highly context-dependent, exerting either tumor-suppressive or oncogenic effects depending on tissue types and disease stage. While their secreted nature positions family members as promising serum or plasma biomarkers, challenges such as ECM protein undruggability, functional heterogeneity, and the absence of upstream regulators have so far precluded direct therapeutic targeting, with no agents advancing to clinical trials. Nonetheless, indirect strategies leveraging their biology show preclinical promise. This review synthesizes current knowledge on SPARC family structure, regulation, and context-specific functions in cancer-TME interactions, emphasizing their dual roles as modulators of progression and resistance. By integrating mechanistic insights with translational advances, we highlight the emerging utility of SPARC family proteins in precision oncology and underscore the need for deeper understanding to enable effective biomarker development and targeted 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.