Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ursolic acid (UA), a natural triterpene acid, is a promising anti-cancer drug due to its inhibitory effect on tumor growth and metastasis. However, clinical translation of UA is limited by its poor water solubility and low bioavailability. To overcome these problems, herein an amphiphilic self-assembly nanodrug composed of UA, lactobionic acid (LA) and low-polyamidoamine (low-PAMAM) dendrimers is developed. This near-spherical nanodrug with a uniform size (~180 nm) demonstrated to have an enhanced cytotoxicity against liver cancer SMMC7721 cells, and could attenuate the migration and adhesion of SMMC7721 cells at non-toxic concentrations by suppressing metastasis-related protein MMP-9 expression. Furthermore, in vivo study indicates that the nanodrug exhibited prolonged circulation time in blood as well as increased AUC, MRT and Cmax, and could effectively inhibit the tumor growth in H22 mice model. Overall, the UA-based nanodrug delivery system reported in the present work represents a novel strategy for targeted tumor therapy.
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PMID:A self-assembly nanodrug delivery system based on amphiphilic low generations of PAMAM dendrimers-ursolic acid conjugate modified by lactobionic acid for HCC targeting therapy. 2912 61

Although gastric cancer (GC) is one of the most common cancers, knowledge of its development, and carcinogenesis is limited. The present study explored the involvement of ceramide synthase 6 (CERS6) in GC carcinogenesis and prognosis. RT-PCR, immunoblotting, and immunohistochemistry were used to examine the expression of CERS6. Transfection and small hairpin RNA technology were used to investigate the effect of CERS6 manipulation on cell proliferation and spread as well as the underlying mechanism. Moreover, xenograft proliferation was employed to explore the influence of CERS6 on tumor growth in animals. It was found that overexpression of CERS6 was significantly correlated with several clinicopathologic parameters and poor disease-free survival. The overexpression and silencing of CERS6 in GC cells facilitated and suppressed cell proliferation and spread as well as xenograft proliferation, respectively. Mechanistic studies further revealed that CERS6 influenced cell proliferation and spread by regulating cell cycle control and metastasis-related protein through the SOCS2/JAK2/STAT3 signaling pathway. Collectively, this study suggests that CERS6 overexpression could be a useful biomarker for predicting the outcomes of GC patients and that CERS6 targeting represents a potential modality for treating GC.
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PMID:Ceramide synthase 6 predicts the prognosis of human gastric cancer: It functions as an oncoprotein by dysregulating the SOCS2/JAK2/STAT3 pathway. 3012 84

Background: Oral squamous cell carcinoma (OSCC) is one of the most common cancers, with high metastasis and mortality. Licochalcone A (LCA) is a chalconoid from the root of Glycyrrhiza inflata, which has anti-tumor, anti-inflammatory, anti-angiogenesis effects in many cancers. However, the mechanism that underlies LCA regulating cell proliferation, migration, and invasion in OSCC remains poorly understood. Methods: LY294002 or insulin-like growth factor 1 (IGF-1) were used to block or stimulate the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) pathway in OSCC cells. Cell proliferation was investigated by MTT assay and proliferating cell nuclear antigen (PCNA) protein level using Western blot. The expression of metastasis-related protein was detected via Western blot. Cell migration and invasion abilities were evaluated by trans-well assay. A murine xenograft model of OSCC was established to investigate the anti-tumor effect of LCA in vivo. Results: Treatment of LCA inhibited cell proliferation in SCC4 and CAL-27 cells. Moreover, PI3K/AKT signaling was blocked by LY294002, and activated by IGF-1. LCA could suppress proliferation, migration, and invasion of OSCC cells, which was similar to the treatment of LY294002. In addition, LCA decreased IGF-1-induced OSCC progression. In a murine xenograft model, LCA treatment protected against tumor growth and metastasis in vivo. Conclusions: LCA might inhibit cell proliferation, migration, and invasion through regulating the PI3K/AKT pathway in OSCC, developing a potential chemotherapeutic agent for OSCC.
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PMID:Licochalcone A inhibits cell proliferation, migration, and invasion through regulating the PI3K/AKT signaling pathway in oral squamous cell carcinoma. 3123 11