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Data · dataset · 2026

Supplementary Figures S1-S6 from Tumor-Secreted ADAMTSL4 Activates Latent TGFβ1 to Drive Cancer Cachexia

Listed in ZivaHub and Deakin Research Online and DMU Figshare — shown once because both records carry DOI 10.1158/2159-8290.34040792

<p>Supplementary Fig. S1.

Description

ADAMTSL4 is enriched in conditioned media of cachexia-inducing cancer cell lines and is associated with systemic metabolic alterations in patients with cancer. Supplementary Fig. S2.

Overexpression of ADAMTSL4 converts non-cachexia-inducing cells into cachexia-inducing cells. Supplementary Fig. S3. Stable knockdown of ADAMTSL4 in cachexia-inducing cells attenuates their muscle-wasting capacity in vitro.

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Supplementary Fig. S4. Stable knockdown of ADAMTSL4 in cachexia-inducing tumor cells attenuates in vitro and in vivo adipocyte wasting and prolongs cachexia-related survival. Supplementary Fig. S5.

ADAMTSL4 targets LAP of latent TGF-β1 complex to promote myotube atrophy via TGF-β latency activation and TGFβR-dependent signaling. Supplementary Fig. S6. ADAMTSL4 induces wasting of murine and human white adipocytes via local activation of TGF-β1–TGFBR1 signaling, without altering circulating TGF-β1 levels.</p>

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Inferred from text
Oncology and carcinogenesis 72%
Provenance · 3 source records, 17 field assertions
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FieldAssertionExtractorEvidence
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concepts[disease].local:disease:cancermapping · figshare dmu ac ukvocabulary-mapper@1.0.0keywords['Cancer']
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