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We are analyzing https://link.springer.com/article/10.1186/s12967-023-04236-x.

Title:
NUCB2/Nesfatin-1 drives breast cancer metastasis through the up-regulation of cholesterol synthesis via the mTORC1 pathway | Journal of Translational Medicine
Description:
Background Reprogramming lipid metabolism for tumor metastasis is essential in breast cancer, and NUCB2/Nesfatin-1 plays a crucial role in regulating energy metabolism. Its high expression is associated with poor prognosis in breast cancer. Here, we studied whether NUCB2/Nesfatin-1 promotes breast cancer metastasis through reprogramming cholesterol metabolism. Methods ELISA was employed to measure the concentration of Nesfatin-1 in the serum of breast cancer patients and the control group. Database analysis suggested that NUCB2/Nesfatin-1 might be acetylated in breast cancer, which was confirmed by treating the breast cancer cells with acetyltransferase inhibitors. Transwell migration and Matrigel invasion assays were conducted, and nude mouse lung metastasis models were established to examine the effect of NUCB2/Nesfatin-1 on breast cancer metastasis in vitro and in vivo. The Affymetrix gene expression chip results were analyzed using IPA software to identify the critical pathway induced by NUCB2/Nesfatin-1. We evaluated the effect of NUCB2/Nesfatin-1 on cholesterol biosynthesis through the mTORC1-SREBP2-HMGCR axis by utilizing mTORC1 inhibitor and rescue experiments. Results NUCB2/Nesfatin-1 was found to be overexpressed in the breast cancer patients, and its overexpression was positively correlated with poor prognosis. NUCB2 was potentially acetylated, leading to high expression in breast cancer. NUCB2/Nesfatin-1 promoted metastasis in vitro and in vivo, while Nesfatin-1 rescued impaired cell metastasis induced by NUCB2 depletion. Mechanistically, NUCB2/Nesfatin-1 upregulated cholesterol synthesis via the mTORC1 signal pathway, contributing to breast cancer migration and metastasis. Conclusions Our findings demonstrate that the NUCB2/Nesfatin-1/mTORC1/SREBP2 signal pathway is critical in regulating cholesterol synthesis, essential for breast cancer metastasis. Thus, NUCB2/Nesfatin-1 might be utilized as a diagnostic tool and also used in cancer therapy for breast cancer in the future.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Does Link.springer.com Make Money? {šŸ’ø}

We don't see any clear sign of profit-making.

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Keywords {šŸ”}

cancer, breast, cell, nucb, cholesterol, nesfatin, pubmed, cells, expression, metastasis, google, scholar, lines, nucbnesfatin, fig, analysis, pathway, cas, invasion, hmgcr, found, results, protein, srebp, central, synthesis, data, stable, migration, signaling, treated, mdamb, western, blot, concentration, shnucbmdamb, mtorc, tumor, patients, potential, article, additional, file, gene, biosynthesis, findings, study, molecular, statistical, tissues,

Topics {āœ’ļø}

3-hydroxy-3-methyl glutaryl-coa reductase shnucb2-mda-mb-231 cell lines camp-response element-binding protein triple-negative breast cancers lkb1/ampk/torc1/zeb1 pathways shnucb2-mda-mb-231 cell line lkb1/ampk/mtorc1/zeb1 pathway [27] nucb2/nesfatin-1/mtorc1/srebp2 signal pathway shnucb2-mda-mb-231 group compared kaplan-meier survival curve ctrl-mda-mb-231 group dna/ca2+ binding protein nucb2/nesfatin-1-induced cholesterol synthesis nucb2 activates mtorc1/srebp2/hmgcr mda-mb-231 cell line smaller lung micro-metastases biol chem hoppe-seyler sterol regulatory element mda-mb-231 cells treated transduce pi3k/akt signaling shnucb2-mda-mb-231 group injected shnucb2-mda-mb-231 akt/ampk/torc2 pathway 4 μg/ml rabbit-igg examined emt-related markers critical rate-limiting enzyme diet-induced insulin resistance hrp-conjugated secondary antibodies control mda-mb-231 cells mtor-stat3 signaling pathway emt-related molecular markers stable cell lines akt-dependent cell growth potential anti-tumor targets cfx96 real-time system acetylated mitochondrial proteins including rate-limiting enzymes mtorc1/srebps/hmgcr axis renal cell carcinoma nucb2/nesfatin-1 upregulates srebp2 nucb2/nesfatin-1—inhibitory effects shnucb2-mda-mb-231 central south university south central region canonical wnt signalling nucb2/nesfatin-1 promoted metastasis shctrl-mda-mb-231 human breast carcinoma article download pdf scrambled mda-mb-231

Questions {ā“}

  • Nucleobindin-2/Nesfatin-1-a new cancer related molecule?

Schema {šŸ—ŗļø}

WebPage:
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         headline:NUCB2/Nesfatin-1 drives breast cancer metastasis through the up-regulation of cholesterol synthesis via the mTORC1 pathway
         description:Reprogramming lipid metabolism for tumor metastasis is essential in breast cancer, and NUCB2/Nesfatin-1 plays a crucial role in regulating energy metabolism. Its high expression is associated with poor prognosis in breast cancer. Here, we studied whether NUCB2/Nesfatin-1 promotes breast cancer metastasis through reprogramming cholesterol metabolism. ELISA was employed to measure the concentration of Nesfatin-1 in the serum of breast cancer patients and the control group. Database analysis suggested that NUCB2/Nesfatin-1 might be acetylated in breast cancer, which was confirmed by treating the breast cancer cells with acetyltransferase inhibitors. Transwell migration and Matrigel invasion assays were conducted, and nude mouse lung metastasis models were established to examine the effect of NUCB2/Nesfatin-1 on breast cancer metastasis in vitro and in vivo. The Affymetrix gene expression chip results were analyzed using IPA software to identify the critical pathway induced by NUCB2/Nesfatin-1. We evaluated the effect of NUCB2/Nesfatin-1 on cholesterol biosynthesis through the mTORC1-SREBP2-HMGCR axis by utilizing mTORC1 inhibitor and rescue experiments. NUCB2/Nesfatin-1 was found to be overexpressed in the breast cancer patients, and its overexpression was positively correlated with poor prognosis. NUCB2 was potentially acetylated, leading to high expression in breast cancer. NUCB2/Nesfatin-1 promoted metastasis in vitro and in vivo, while Nesfatin-1 rescued impaired cell metastasis induced by NUCB2 depletion. Mechanistically, NUCB2/Nesfatin-1 upregulated cholesterol synthesis via the mTORC1 signal pathway, contributing to breast cancer migration and metastasis. Our findings demonstrate that the NUCB2/Nesfatin-1/mTORC1/SREBP2 signal pathway is critical in regulating cholesterol synthesis, essential for breast cancer metastasis. Thus, NUCB2/Nesfatin-1 might be utilized as a diagnostic tool and also used in cancer therapy for breast cancer in the future.
         datePublished:2023-06-05T00:00:00Z
         dateModified:2023-08-03T00:00:00Z
         pageStart:1
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            Cholesterol synthesis
            Metastasis
            Nucleobindin-2/Nesfatin-1
            Biomedicine
            general
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      headline:NUCB2/Nesfatin-1 drives breast cancer metastasis through the up-regulation of cholesterol synthesis via the mTORC1 pathway
      description:Reprogramming lipid metabolism for tumor metastasis is essential in breast cancer, and NUCB2/Nesfatin-1 plays a crucial role in regulating energy metabolism. Its high expression is associated with poor prognosis in breast cancer. Here, we studied whether NUCB2/Nesfatin-1 promotes breast cancer metastasis through reprogramming cholesterol metabolism. ELISA was employed to measure the concentration of Nesfatin-1 in the serum of breast cancer patients and the control group. Database analysis suggested that NUCB2/Nesfatin-1 might be acetylated in breast cancer, which was confirmed by treating the breast cancer cells with acetyltransferase inhibitors. Transwell migration and Matrigel invasion assays were conducted, and nude mouse lung metastasis models were established to examine the effect of NUCB2/Nesfatin-1 on breast cancer metastasis in vitro and in vivo. The Affymetrix gene expression chip results were analyzed using IPA software to identify the critical pathway induced by NUCB2/Nesfatin-1. We evaluated the effect of NUCB2/Nesfatin-1 on cholesterol biosynthesis through the mTORC1-SREBP2-HMGCR axis by utilizing mTORC1 inhibitor and rescue experiments. NUCB2/Nesfatin-1 was found to be overexpressed in the breast cancer patients, and its overexpression was positively correlated with poor prognosis. NUCB2 was potentially acetylated, leading to high expression in breast cancer. NUCB2/Nesfatin-1 promoted metastasis in vitro and in vivo, while Nesfatin-1 rescued impaired cell metastasis induced by NUCB2 depletion. Mechanistically, NUCB2/Nesfatin-1 upregulated cholesterol synthesis via the mTORC1 signal pathway, contributing to breast cancer migration and metastasis. Our findings demonstrate that the NUCB2/Nesfatin-1/mTORC1/SREBP2 signal pathway is critical in regulating cholesterol synthesis, essential for breast cancer metastasis. Thus, NUCB2/Nesfatin-1 might be utilized as a diagnostic tool and also used in cancer therapy for breast cancer in the future.
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      dateModified:2023-08-03T00:00:00Z
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         Cholesterol synthesis
         Metastasis
         Nucleobindin-2/Nesfatin-1
         Biomedicine
         general
         Medicine/Public Health
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                     type:PostalAddress
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                     name:Hunan Normal University School of Medicine, Changsha, China
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                     name:Department of Immunology, College of Basic Medical Sciences, Central South University, Changsha, China
                     type:PostalAddress
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                  name:Guangzhou Medical University, Guangdong Provincial Clinical Research Center for Child Health, National Children’s Medical Center for South Central Region
                  address:
                     name:Department of Pathology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangdong Provincial Clinical Research Center for Child Health, National Children’s Medical Center for South Central Region, Guangzhou, China
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      name:Liang Zeng
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            name:Guangzhou Medical University, Guangdong Provincial Clinical Research Center for Child Health, National Children’s Medical Center for South Central Region
            address:
               name:Department of Pathology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangdong Provincial Clinical Research Center for Child Health, National Children’s Medical Center for South Central Region, Guangzhou, China
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      name:Department of Immunology, College of Basic Medical Sciences, Central South University, Changsha, China
      name:Department of Immunology, College of Basic Medical Sciences, Central South University, Changsha, China
      name:Department of General Surgery, The Xiangya Hospital, Central South University, Changsha, China
      name:Department of Immunology, College of Basic Medical Sciences, Central South University, Changsha, China
      name:Hunan Normal University School of Medicine, Changsha, China
      name:Department of Immunology, College of Basic Medical Sciences, Central South University, Changsha, China
      name:Department of Pathology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangdong Provincial Clinical Research Center for Child Health, National Children’s Medical Center for South Central Region, Guangzhou, China

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