Yeast extract inhibits the proliferation of renal cell carcinoma cells via regulation of iron metabolism

The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome 'X&#...

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Published inMolecular medicine reports Vol. 20; no. 4; pp. 3933 - 3941
Main Authors Moon, Daeun, Kim, Jinu, Yoon, Sang‑Pil
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.10.2019
Spandidos Publications UK Ltd
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Abstract The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome 'X'. The antitumor effects of RCM were investigated for all ingredients of RCM, and the results revealed that yeast extract could be a candidate for the ingredient driving this phenomenon. Further experiments including MTT assay, cell counting, cell death analysis, cell cycle analysis and western blotting were conducted with yeast extract on renal cell carcinoma cells (Caki‑1 and Caki‑2) and normal human proximal tubular cells (HK‑2). As a result, yeast extract exhibited dose‑dependent antitumor effects on Caki‑1 and Caki‑2, but only slight effects on HK‑2. In addition, yeast extract only exhibited slight effects on necrosis, autophagy, or apoptosis of Caki‑1 and Caki‑2. Yeast extract produced cell cycle arrest with an increased G0/G1 fraction and a decreased S fraction, and this was considered to be related to the decreased cyclin D1. Although yeast extract treatment increased anti‑oxidant activities, the antitumor effects of yeast extract were also related to iron metabolism, based on the decreased transferrin receptor and increased ferritin. In addition, decreased GPX4 may be related to iron‑dependent cell death, particularly in Caki‑2. These results revealed that yeast extract may inhibit proliferation of renal cell carcinoma cells by regulating iron metabolism. Since an increased iron requirement is a classic phenomenon of cancer cells, yeast extract may be a candidate for adjuvant treatment of renal cell carcinoma.
AbstractList The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome ‘X’. The antitumor effects of RCM were investigated for all ingredients of RCM, and the results revealed that yeast extract could be a candidate for the ingredient driving this phenomenon. Further experiments including MTT assay, cell counting, cell death analysis, cell cycle analysis and western blotting were conducted with yeast extract on renal cell carcinoma cells (Caki-1 and Caki-2) and normal human proximal tubular cells (HK-2). As a result, yeast extract exhibited dose-dependent antitumor effects on Caki-1 and Caki-2, but only slight effects on HK-2. In addition, yeast extract only exhibited slight effects on necrosis, autophagy, or apoptosis of Caki-1 and Caki-2. Yeast extract produced cell cycle arrest with an increased G0/G1 fraction and a decreased S fraction, and this was considered to be related to the decreased cyclin D1. Although yeast extract treatment increased anti-oxidant activities, the antitumor effects of yeast extract were also related to iron metabolism, based on the decreased transferrin receptor and increased ferritin. In addition, decreased GPX4 may be related to iron-dependent cell death, particularly in Caki-2. These results revealed that yeast extract may inhibit proliferation of renal cell carcinoma cells by regulating iron metabolism. Since an increased iron requirement is a classic phenomenon of cancer cells, yeast extract may be a candidate for adjuvant treatment of renal cell carcinoma.
The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome 'X'. The antitumor effects of RCM were investigated for all ingredients of RCM, and the results revealed that yeast extract could be a candidate for the ingredient driving this phenomenon. Further experiments including MTT assay, cell counting, cell death analysis, cell cycle analysis and western blotting were conducted with yeast extract on renal cell carcinoma cells (Caki-1 and Caki-2) and normal human proximal tubular cells (HK-2). As a result, yeast extract exhibited dose-dependent antitumor effects on Caki-1 and Caki-2, but only slight effects on HK-2. In addition, yeast extract only exhibited slight effects on necrosis, autophagy, or apoptosis of Caki-1 and Caki-2. Yeast extract produced cell cycle arrest with an increased [G.sub.0]/[G.sub.1] fraction and a decreased S fraction, and this was considered to be related to the decreased cyclin D1. Although yeast extract treatment increased anti-oxidant activities, the antitumor effects of yeast extract were also related to iron metabolism, based on the decreased transferrin receptor and increased ferritin. In addition, decreased GPX4 may be related to iron-dependent cell death, particularly in Caki-2. These results revealed that yeast extract may inhibit proliferation of renal cell carcinoma cells by regulating iron metabolism. Since an increased iron requirement is a classic phenomenon of cancer cells, yeast extract may be a candidate for adjuvant treatment of renal cell carcinoma. Key words: yeast extract, renal cell carcinoma, iron, cell cycle, ferroptosis
The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome 'X'. The antitumor effects of RCM were investigated for all ingredients of RCM, and the results revealed that yeast extract could be a candidate for the ingredient driving this phenomenon. Further experiments including MTT assay, cell counting, cell death analysis, cell cycle analysis and western blotting were conducted with yeast extract on renal cell carcinoma cells (Caki‑1 and Caki‑2) and normal human proximal tubular cells (HK‑2). As a result, yeast extract exhibited dose‑dependent antitumor effects on Caki‑1 and Caki‑2, but only slight effects on HK‑2. In addition, yeast extract only exhibited slight effects on necrosis, autophagy, or apoptosis of Caki‑1 and Caki‑2. Yeast extract produced cell cycle arrest with an increased G0/G1 fraction and a decreased S fraction, and this was considered to be related to the decreased cyclin D1. Although yeast extract treatment increased anti‑oxidant activities, the antitumor effects of yeast extract were also related to iron metabolism, based on the decreased transferrin receptor and increased ferritin. In addition, decreased GPX4 may be related to iron‑dependent cell death, particularly in Caki‑2. These results revealed that yeast extract may inhibit proliferation of renal cell carcinoma cells by regulating iron metabolism. Since an increased iron requirement is a classic phenomenon of cancer cells, yeast extract may be a candidate for adjuvant treatment of renal cell carcinoma.The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome 'X'. The antitumor effects of RCM were investigated for all ingredients of RCM, and the results revealed that yeast extract could be a candidate for the ingredient driving this phenomenon. Further experiments including MTT assay, cell counting, cell death analysis, cell cycle analysis and western blotting were conducted with yeast extract on renal cell carcinoma cells (Caki‑1 and Caki‑2) and normal human proximal tubular cells (HK‑2). As a result, yeast extract exhibited dose‑dependent antitumor effects on Caki‑1 and Caki‑2, but only slight effects on HK‑2. In addition, yeast extract only exhibited slight effects on necrosis, autophagy, or apoptosis of Caki‑1 and Caki‑2. Yeast extract produced cell cycle arrest with an increased G0/G1 fraction and a decreased S fraction, and this was considered to be related to the decreased cyclin D1. Although yeast extract treatment increased anti‑oxidant activities, the antitumor effects of yeast extract were also related to iron metabolism, based on the decreased transferrin receptor and increased ferritin. In addition, decreased GPX4 may be related to iron‑dependent cell death, particularly in Caki‑2. These results revealed that yeast extract may inhibit proliferation of renal cell carcinoma cells by regulating iron metabolism. Since an increased iron requirement is a classic phenomenon of cancer cells, yeast extract may be a candidate for adjuvant treatment of renal cell carcinoma.
The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome 'X'. The antitumor effects of RCM were investigated for all ingredients of RCM, and the results revealed that yeast extract could be a candidate for the ingredient driving this phenomenon. Further experiments including MTT assay, cell counting, cell death analysis, cell cycle analysis and western blotting were conducted with yeast extract on renal cell carcinoma cells (Caki-1 and Caki-2) and normal human proximal tubular cells (HK-2). As a result, yeast extract exhibited dose-dependent antitumor effects on Caki-1 and Caki-2, but only slight effects on HK-2. In addition, yeast extract only exhibited slight effects on necrosis, autophagy, or apoptosis of Caki-1 and Caki-2. Yeast extract produced cell cycle arrest with an increased [G.sub.0]/[G.sub.1] fraction and a decreased S fraction, and this was considered to be related to the decreased cyclin D1. Although yeast extract treatment increased anti-oxidant activities, the antitumor effects of yeast extract were also related to iron metabolism, based on the decreased transferrin receptor and increased ferritin. In addition, decreased GPX4 may be related to iron-dependent cell death, particularly in Caki-2. These results revealed that yeast extract may inhibit proliferation of renal cell carcinoma cells by regulating iron metabolism. Since an increased iron requirement is a classic phenomenon of cancer cells, yeast extract may be a candidate for adjuvant treatment of renal cell carcinoma.
The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced clostridium media (RCM) for microbiome culture, exerts antitumor effects on renal cell carcinoma cells when compared to the microbiome 'X'. The antitumor effects of RCM were investigated for all ingredients of RCM, and the results revealed that yeast extract could be a candidate for the ingredient driving this phenomenon. Further experiments including MTT assay, cell counting, cell death analysis, cell cycle analysis and western blotting were conducted with yeast extract on renal cell carcinoma cells (Caki‑1 and Caki‑2) and normal human proximal tubular cells (HK‑2). As a result, yeast extract exhibited dose‑dependent antitumor effects on Caki‑1 and Caki‑2, but only slight effects on HK‑2. In addition, yeast extract only exhibited slight effects on necrosis, autophagy, or apoptosis of Caki‑1 and Caki‑2. Yeast extract produced cell cycle arrest with an increased G0/G1 fraction and a decreased S fraction, and this was considered to be related to the decreased cyclin D1. Although yeast extract treatment increased anti‑oxidant activities, the antitumor effects of yeast extract were also related to iron metabolism, based on the decreased transferrin receptor and increased ferritin. In addition, decreased GPX4 may be related to iron‑dependent cell death, particularly in Caki‑2. These results revealed that yeast extract may inhibit proliferation of renal cell carcinoma cells by regulating iron metabolism. Since an increased iron requirement is a classic phenomenon of cancer cells, yeast extract may be a candidate for adjuvant treatment of renal cell carcinoma.
Audience Academic
Author Moon, Daeun
Yoon, Sang‑Pil
Kim, Jinu
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  fullname: Yoon, Sang‑Pil
  organization: Department of Anatomy, School of Medicine, Jeju National University, Jeju 63243, Republic of Korea
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Snippet The microbiome has recently attracted research interest in a variety of subjects, including cancer. In the present study, it was determined that reinforced...
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SubjectTerms Adjuvant treatment
Antineoplastic Agents - chemistry
Antineoplastic Agents - pharmacology
Antitumor activity
Apoptosis
Autophagy
Cancer
Carcinoma, Renal cell
Carcinoma, Renal Cell - metabolism
Carcinoma, Renal Cell - microbiology
Carcinoma, Renal Cell - therapy
Cell culture
Cell cycle
Cell Cycle Checkpoints - drug effects
Cell death
Cell Line
Cell Line, Tumor
Cell proliferation
Cell Proliferation - drug effects
Chemotherapy
Comparative analysis
Culture Media - chemistry
Culture Media - pharmacology
Cyclin D1
Fatty acids
Ferritin
Ferroptosis
Flow cytometry
Gastrointestinal Microbiome
Homeostasis
Humans
Ingredients
Instrument industry
Iron
Iron - metabolism
Kidney cancer
Kidney diseases
Kidney Neoplasms - metabolism
Kidney Neoplasms - microbiology
Kidney Neoplasms - therapy
Kinases
Metastasis
Microbiomes
Microbiota
Phagocytosis
Pharmaceutical industry
Renal cell carcinoma
Transferrins
Western blotting
Yeast
Yeasts - chemistry
Yeasts - physiology
Title Yeast extract inhibits the proliferation of renal cell carcinoma cells via regulation of iron metabolism
URI https://www.ncbi.nlm.nih.gov/pubmed/31432187
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Volume 20
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