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A Review on Protein and Cancer ; Etiology, Metabolism and Management


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Altered metabolism is one of the hallmarks of cancer cells. Cell cycling and protein synthesis are both key
physiological tasks for cancer cells. In recent years, interest has been renewed as clear that many of the signaling
pathways that are affected by genetic mutations and the tumor microenvironment have a profound effect on core
metabolism of cancer cells. Metabolic alterations in cancer cells are numerous and include aerobic glycolysis,
reduced oxidative phosphorylation and the increased generation of biosynthetic intermediates needed for cell
growth and proliferation. Furthermore, accelerated protein turnover seen in many cancer patients and whole body
protein turnover is increased with advancing stage of disease. Cancer cells alter their consumption and the way
they process sugars, fats, amino acids and other energy sources to satisfy the demands of continuous proliferation.
The possible effects of specific amino acid, methionine, asparagine, arginine, tyrosine and glutamine, etc. on
protein cancer metabolism are discussed. Evidences confirm a contribution of proteins in all cancer stages and
describe metabolism of protein in cancer and how amino acids can be targeted to management or initially prevent
different types of cancer. Several studies suggest that people who eat more red meat have higher risk for
developing colorectal cancer than those who eat less red meat, but avoiding processed meats is even more
important for cancer prevention. In this review we summarize the role of proteins in cancer etiology, metabolism,
its complication, prevention and treatments.

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A Review on Protein and Cancer ; Etiology, Metabolism and Management

  1. 1. A Review on Protein and Cancer: Etiology, Metabolism and Management By: Abdel-Rahman Ragab 4th level Student Zoology Chemistry department Under Supervision of;Prof Dr : Adel Abdel-Moneim
  2. 2. publications 1-Abdel-Moneim A,Ragab A,Magdy A,Mohamed A E,Amged R (2016):CANCER METABOLISM,Lap Lambert Acaedemic Publishing ,Germany. 2-Adel Abdel-Moneim & Abdel-Rahman Ragab. CANCER PROTEIN METABOLISM: REVIEW ON ETIOLOGY, PROGRESSION AND MANAGEMENT. EJBPS 2016, 3 (6), 63-80. Abdel-Rahman Ragab 2016
  3. 3. contents 1-Introduction. 2-Abnormal metabolism etiological role. 3-Abnormal metabolism during cancer development. 4-Complications of cancer. 5-Prevention and treatment of cancer. 6-Conclusion. Abdel-Rahman Ragab 2016
  4. 4. Introduction cancer classification Cancer classification According to site of origin: Ex:breast,pr ostate,lung, Liver and brain cancer According to behavior :benign &malignant According to tissue type (anatomy): Carcinoma, Sarcoma, Lymphoma, Leukemias, Myeloma And Mixed types According to grade (histological classification): Grade 1,2,3,4 and 5 According to clinical stage: Stage 0,1,2,3 and 4Abdel-Rahman Ragab 2016
  5. 5. Introduction cancer diagnosis Morphological methods Biomarker genes or proteins:ex BRCA1 / BRCA2 (Breast/Ovaria n Cancer) Sampling methods: (Incisional,Excisional, Fine needle aspiration) biobsy,Cytology, Bone marrow aspiration,Endoscopic procedures Molecular techniques: Pcr, FISH, SKI, DNA microarrays, Flow cytometry,EM and IHC Imaging diagnosis:CT,MR I scan, X-rays, Mammography, Nuclear medicine scans, Ultrasound Diagnostic techniques Abdel-RahmanRagab 2016
  6. 6. Aim of work The goal of the current review is elucidate the role of abnormal protein metabolism in cancer states: etiology, developing, progression, and cancer complication related to protein metabolism. Moreover, the treatment and dietary guidelines for prevention using safe protein natural products. Abdel-Rahman Ragab 2016
  7. 7. Protein metabolism in normal cells
  8. 8. abnormal metabolism etiological role. Loss of due to P53 mutation Mutation ↓ oncogene . glycine N- methyltransfe -rase dysfynction→ hypermethyla -tion→ activation Ras →liver cancer arginase dysfunction→ colon cancer Transglutami- nase 4 differential splicing mRNA→ prostate cancer + ↑temp + certain sugar→ acrylamide Hypermethyl -ation suppressor gene (mutation) Methionine: Asparagine Glutamine: Arginine: Glycine: proto- oncogene apoptosis
  9. 9. Digestion and absorption in cancer Mechanical Digestive abnormalities Lack of appetite & reduced Food intake Cancer Associated Weight loss maldigestion malabsorption Patient suffer from: Dysgeusia, Early satiation, Nausea, Dysphagia, Odynophagia mucotis, Constipation, Diarrhea, Gastric infiltration and bowel
  10. 10. Protein Metabolism during cancer proliferation Glutamine 2nd principal nutrient Oxidn (NADH &FADH2) Provide N (pyrines,pyrimidine,nonessential a.a Import essential a.a ↑c-myc ↓Rb akg→TCA F.a.a unavailable extracellular protein lysis entosis of living cells phagocytosis of apoptotic bodies Arginine 4 N ,precursor proline Albumin lysis to F.A.A for N &E Tryptophan catabolism suppress antitumor immune response Warburg effect cancer have ↑rate glucose consumption reverse Warburg tumor consume (lactate,ketone bodies,glutamin,F.A to produce E increase A.A consumption→overexpression cell surface receptor Metabolism during cancer development
  11. 11. Cancer complication Include:pain,fatigue,difficulty breathing,nausea,diarrhea,constipation,nervous system problem,systemic disorder,angiogenesis,metastasis and cachexia.
  12. 12. metastasis Means: cancer spread from organ to another through b.v. or lymph ex:lung→brain Metalloproteinases: degrade the basement membrane. Fibronectin: break down (ECM). Osteopontin (OPN) Galectin-3 Transforming growth factor-β (TGF-β) Fibroblast activation protein α Actin EMT Type III Integrins Mammalian translationally controlled tumor protein (TCTP)
  13. 13. Cachexia Means: Catabolic process include muscle wasting with or without fat loss and cannot be fully reversed. Tumor inflammation Cytokine: IL2,IL6 and TNF- alpha Hypothalamus (appetite center) Anorexia and Continuous daily protein turn over ↓ plasma anabolic hormone Testosterone GH Insulin or its sensitivity of sk. muscle proteolytic pathways Ex:lysosomal system Muscle apoptosis cachexia N.B.Cachexia cause loss of respiratory muscle function will lead to respiratory failure w lead to death.
  14. 14. prevention Limit Consumption of Processed Meats and Red Meats. •High intake associated with Colorectal ,colon, rectal and breast cancer •Minimize consumption of processed meats such as bacon, sausage, luncheon meats and hot dogs •choose fish, poultry, or beans as an alternative to red meat •prepare meat, poultry, and fish by baking,broiling,or poaching rather than by frying or charboilling Use Soy Products •good alternative to meat •have weak estrogenic activity and may protect against hormone-dependent cancers •decrease the risk of cancers of the breast ,prostate,or endometrium Use dairy product •Higher intakes of milk and total dairy products •Reduce risk of colon For colorectal cancer and breast cancer
  15. 15. treatment drugmechanismtarget nutlinInhibit p53-MDM2 interaction p53 azaserineUsed for side effects of cancerchemotherapy Glutamine Clinical trials---------------------------------------a.a metabolic enzyme gefitinibInterfere with a specific molecular target ex: ErbB1 (EGFR) Tyrosine kinases agents
  16. 16. Cachexia treatment Testosterone Increase muscle mass by reducing loss of sk. Muscle a.a Recombinant GH improve nutritional status Gherlin improve lean and total body mass Insulin Anabolic to sk. Muscle &inhibits lipolysis
  17. 17. conclusion Tumorigenesis is dependent on the reprogramming of cellular metabolism consequence of oncogenic mutations. A common feature of cancer cell metabolism is the ability to acquire necessary nutrients from a frequently nutrient-poor environment and utilize these nutrients to both maintain viability and build new biomass. There is clearly a great deal to learned about the interrelation of glucose and glutamine metabolism in support of cell growth and proliferation, and how nutrient metabolism is coordinated to support successful cell growth/proliferation. Therefore, the ultimate goal is to design treatment strategies that affect several proteins metabolism pathways that slow tumor progression, improve the response to therapy and result in a positive clinical outcome. Evidences reviewed confirm a contribution of proteins in all cancer stages and describe metabolism of protein in cancer and how several amino acid can be targeted to management or initially prevent different types of cancer. Moreover, if we are not able to eradicate cancer in the future decades, there is still much great effort should be done to prevent cancer occurrence with healthy diet and change our lifestyle.
  18. 18. Acknowledgment My foremost and greatest gratitude and indebtedness go ALLAH for his guidance and support in my all life and lightening my path to finish this thesis. I am sincerely grateful to Prof.Dr.Adel Abdel-Moneim Ahmed ,professor of physiology ,department of zoology ,faculty of science ,beni-suef university for his choice of the review point ,fruitful direction ,accurate revision of this work ,valuable and constructive discussion and his kind encouragement and interest through the entire work. Words will never be able to express my deepest gratitude to my parents, brothers and my sister whom give me loved and devote all their comfort for me to overcome the hard times. Last but not least my special and warmest acknowledgment go to my parents whom the joy of our life and the light of our eyes. Abdel-Rahman Ragab Qoureny