2. Warburg assumed that cancer cells required fermentative glucose metabolism due to mitochondrial dysfunction. This notion has since been largely proven incorrect. Instead, there have been a number of proposed rationales as to how the Warburg effect/aerobic glycolysis supports (cancer) cell proliferation. Identify and explain two such hypotheses and why they may not serve as complete mechanistic explanations. Limit your responses to 4 sentences per hypothesis. -it allows cancer cell to make biosynthetic building blocks (nucleotide, lipid, amino acid) more efficiently. -increased demand for NAD+ drives aerobic glycolysis.

2. Warburg assumed that cancer cells required fermentative glucose metabolism due to mitochondrial dysfunction. This notion has since been largely proven incorrect. Instead, there have been a number of proposed rationales as to how the Warburg effect/aerobic glycolysis supports (cancer) cell proliferation. Identify and explain two such hypotheses and why they may not serve as complete mechanistic explanations. Limit your responses to 4 sentences per hypothesis. -it allows cancer cell to make biosynthetic building blocks (nucleotide, lipid, amino acid) more efficiently. -increased demand for NAD+ drives aerobic glycolysis.

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter2: Cell Physiology

Section: Chapter Questions

Problem 3TAHL

See similar textbooks

Similar questions

Discuss/explain, in details, the relationship between cell viability and cell vitality and cell apoptosis as suggested by neutral red uptake,
Provide three examples of changes in glycolysis/TCA that lead to increased biosynthesis, and, therefore, cancer cell proliferation.
Same question but two different sections
e During apoptosis, rates of protein degradation activity. Select one: a. decrease, decrease b. increase, decrease c. increase, increase d. decrease, increase Cycle HW due y Nov 3rd at 5pm Jump to... ( caused by protease Next page cancer stem cells ►
this is a molecular cell biology question
Very briefly, explain how increased cytoplasmic IP3 levels can then increase cytoplasmic calcium (Ca2+) levels.
Do you know #4 ?
Need help, please. I know the answer isn't mitotic spindle or secretory and endocytic vesicle transport. I think the answer is option C, axon stiffening, and neurotransmitter vesicle transport, but I am not 100% sure. What function of the microtubule motor proteins dynein and kinesin is blocked by the use of colchicine to treat gout? Select one: O a. mitotic spindle b. secretory and endocytic vesicle transport c. axon stiffening and neurotransmitter vesicle transport O d. ER, Golgi, and mitochondria movement
Autophagy Is Required for PKA Activation and Cell Viability upon GlucoseStarvation. The functional relationship between PKA and autophagyis largely unclear. Because PKA controls cell metabolism particularly related to glucose status (21–23), we first examined the relationship between autophagy and PKA activity in the control of cellmetabolism with glucose limitation. We found that in addition toactivating autophagy, glucose starvation also induced the phosphorylation of cAMP response element-binding (p-CREB), a wellknown PKA substrate, indicative of elevated PKA activity in bothHEK293T and HCT116 cells. In contrast, disruption of autophagyby deletion of essential autophagy gene Atg7 or Atg14 abolished theincrease of p-CREB levels in the above cells (SI Appendix, Fig.S1 A, B, D, and E), suggesting that inactivation of autophagy suppresses PKA activity in response to energy shortage. Moreover, lossof Atg7 or Atg14 accelerated cell death in response to glucosestarvation (SI Appendix, Fig.…
Answer: a and b .from given options.Do explain shortly.Thanks
. Leukemia is a neoplastic (cancerous) proliferation of white blood cells. Clinicians are currently testing deoxycoformycin, an adenosine deaminase inhibitor, as a possible antileukemic agent. Why might one expect this therapy to be effective?
In acute lymphoblastic leukemia, the cancerous white blood cells typically lack the enzyme asparagine synthetase. Why is the administration of asparaginase an eff ective therapy for this type of cancer?