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We are analyzing https://link.springer.com/article/10.1007/s10495-017-1366-2.

Title:
Fatty acid synthase regulates the chemosensitivity of breast cancer cells to cisplatin-induced apoptosis | Apoptosis
Description:
Fatty acid synthase (FASN) is a key enzyme in fat biosynthesis that is over-expressed in advanced breast cancer stages. Cisplatin (CDDP) is a platinum-based drug used in the treatment of certain types of this disease. Although it was shown that FASN inhibition induced apoptosis by enhancing the cytotoxicity of certain drugs in breast cancer, its role in regulating the chemosensitivity of different types of breast cancer cells to CDDP-induced apoptosis is not established yet. Therefore, two different breast cancer cell lines; triple negative breast cancer (TNBC; MDA-MB-231) and triple positive breast cancer (TPBC; BT-474) cells were used to examine such role. We show that TNBC cells had naturally less fat content than TPBC cells. Subsequently, the fat content increased in both cells when treated with Palmitate rather than Oleate, whereas both fatty acids produced apoptotic ultra-structural effects and attenuated FASN expression. However, Oleate increased FASN expression in TPBC cells. CDDP decreased FASN expression and increased apoptosis in TNBC cells. These effects were further enhanced by combining CDDP with fatty acids. We also illustrate that the inhibition of FASN by either siRNA or exogenous inhibitor decreased CDDP-induced apoptosis in TPBC cells suggesting its role as an apoptotic factor, while an opposite finding was observed in TNBC cells when siRNA and fatty acids were used, suggesting its role as a survival factor. To our knowledge, we are the first to demonstrate a dual role of FASN in CDDP-induced apoptosis in breast cancer cells and how it can modulate their chemosensitivity.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Health & Fitness
  • Science
  • Education

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

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


Based on our best estimate, this website will receive around 7,626,932 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We're unsure how the site profits.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {πŸ”}

cancer, article, google, scholar, pubmed, breast, fatty, cells, acid, cas, synthase, apoptosis, role, central, cell, content, fasn, human, oncol, acids, effects, access, res, menendez, colomer, privacy, cookies, chemosensitivity, albahlani, aladawi, inhibition, tnbc, palmitate, oleate, dual, growth, clin, lupu, health, sciences, publish, research, search, drug, cytotoxicity, mdamb, tpbc, targeting, triplenegative, proliferation,

Topics {βœ’οΈ}

month download article/chapter 2/neu-positive breast cancer fatty-acid synthase inhibition protein-coupled receptor gpr40 triple-negative breast cancer calcium/calpain-dependent mechanism 2/neu-overexpressing breast cancer anchorage-independent growth transition fatty acid synthase cisplatin-induced apoptosis published moza al-adawi article al-bahlani nadia al-abri article apoptosis aims fatty acid modulation breast cancer subtypes full article pdf shadia al-bahlani breast cancer cells estrogen receptor signaling ovarian cancer cells cancer gene discovery cddp-induced apoptosis privacy choices/manage cookies cisplatin-induced apoptosis related subjects targeting cellular metabolism platinum-based chemotherapy rapid tumor growth cytotoxic effects modulated breast cancer survival de la rosa adipose tissue global cancer statistics improve cancer therapeutics fatty acids breast cancer chemosensitivity platinum-based drug attenuated fasn expression cancer chemoprevention al-adawi european economic area mda-mb-231 developing retinal neuroepithelium signaling molecules implicated synergistically enhances taxol acetyl-coa carboxylase acute lymphoblastic leukemia sultan qaboos university hanaa al-lawati

Questions {❓}

  • Alarmo E, Kallioniemi A (2010) Bone morphogenetic proteins in breast cancer: dual role in tumourigenesis?
  • Menendez J, Colomer R, Lupu R (2005) Why does tumor-associated fatty acid synthase (oncogenic antigen-519) ignore dietary fatty acids?

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Fatty acid synthase regulates the chemosensitivity of breast cancer cells to cisplatin-induced apoptosis
         description:Fatty acid synthase (FASN) is a key enzyme in fat biosynthesis that is over-expressed in advanced breast cancer stages. Cisplatin (CDDP) is a platinum-based drug used in the treatment of certain types of this disease. Although it was shown that FASN inhibition induced apoptosis by enhancing the cytotoxicity of certain drugs in breast cancer, its role in regulating the chemosensitivity of different types of breast cancer cells to CDDP-induced apoptosis is not established yet. Therefore, two different breast cancer cell lines; triple negative breast cancer (TNBC; MDA-MB-231) and triple positive breast cancer (TPBC; BT-474) cells were used to examine such role. We show that TNBC cells had naturally less fat content than TPBC cells. Subsequently, the fat content increased in both cells when treated with Palmitate rather than Oleate, whereas both fatty acids produced apoptotic ultra-structural effects and attenuated FASN expression. However, Oleate increased FASN expression in TPBC cells. CDDP decreased FASN expression and increased apoptosis in TNBC cells. These effects were further enhanced by combining CDDP with fatty acids. We also illustrate that the inhibition of FASN by either siRNA or exogenous inhibitor decreased CDDP-induced apoptosis in TPBC cells suggesting its role as an apoptotic factor, while an opposite finding was observed in TNBC cells when siRNA and fatty acids were used, suggesting its role as a survival factor. To our knowledge, we are the first to demonstrate a dual role of FASN in CDDP-induced apoptosis in breast cancer cells and how it can modulate their chemosensitivity.
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      headline:Fatty acid synthase regulates the chemosensitivity of breast cancer cells to cisplatin-induced apoptosis
      description:Fatty acid synthase (FASN) is a key enzyme in fat biosynthesis that is over-expressed in advanced breast cancer stages. Cisplatin (CDDP) is a platinum-based drug used in the treatment of certain types of this disease. Although it was shown that FASN inhibition induced apoptosis by enhancing the cytotoxicity of certain drugs in breast cancer, its role in regulating the chemosensitivity of different types of breast cancer cells to CDDP-induced apoptosis is not established yet. Therefore, two different breast cancer cell lines; triple negative breast cancer (TNBC; MDA-MB-231) and triple positive breast cancer (TPBC; BT-474) cells were used to examine such role. We show that TNBC cells had naturally less fat content than TPBC cells. Subsequently, the fat content increased in both cells when treated with Palmitate rather than Oleate, whereas both fatty acids produced apoptotic ultra-structural effects and attenuated FASN expression. However, Oleate increased FASN expression in TPBC cells. CDDP decreased FASN expression and increased apoptosis in TNBC cells. These effects were further enhanced by combining CDDP with fatty acids. We also illustrate that the inhibition of FASN by either siRNA or exogenous inhibitor decreased CDDP-induced apoptosis in TPBC cells suggesting its role as an apoptotic factor, while an opposite finding was observed in TNBC cells when siRNA and fatty acids were used, suggesting its role as a survival factor. To our knowledge, we are the first to demonstrate a dual role of FASN in CDDP-induced apoptosis in breast cancer cells and how it can modulate their chemosensitivity.
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         Biochemistry
         general
         Virology
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