By inspection of the Western Blots shown in Figure 3 Panels C and D, why did the authors decide to probe for tubulin?

Refer to Hervieu et al. (2020) for Questions #1-5.
Question #1: In figure 1, M1268T refers to:
A.a constitutively active MET mutant
B.Wild type non-cancerous murine model
C.a constitutively active mTOR mutant
D.a naturally occurring non-cancerous tyrosine kinase
2.
By inspection of the Western Blots shown in Figure 1D, the absence of a P-AKT band with MET inhibition in mutant cells suggests that:
A. Mutant MET inactivates AKT.
B. MET is downstream of AKT.
C. Mutant MET activates AKT.
D. The relative amounts of P-AKT are comparable in DMSO and LY treated samples from mutant MET cells.
3.
By inspection of the Western Blots shown in Figure 3 Panels C and D, why did the authors decide to probe for tubulin?
A. To show that all samples were loaded equally.
B. To show the involvement of tubulin in the MET-PI3K-AKT pathway.
C. To verify that p70-S6K is indeed upstream of mTOR.
D. To prove that there are proteins that are not effected by DMSO treatment.
4.
In Figure 4, the authors use RNAi to:
A. As a way to increase expression of Rac1 to show its effects on mTOR-mediated oncogenic MET-driven anchorage independent growth.
B. To show that decreased levels of Rac1 stimulates P-p70-S6K.
C. To show that decreased levels of Rac1 stimulates MET.
D. As a way to knock down expression of Rac1 to show its effects on mTOR-mediated oncogenic MET-driven anchorage independent growth.

5.The main findings of this paper:
A. Proves only non-oncogenic MET promotes anchorage-independent growth through the Rac1-mTOR pathway.
B. Showed that Rac1 regulates both MET-dependent cell migration and anchorage-independent growth whereas PI3K is involved in MET-dependent cell migration only.
C. Demonstrated that Rac1 mediates anchorage-independent growth of MET-mutant cells which is dependent on GTPase activity.
D. Shows that RTKs do not play a role in tumor growth and metastasis.

6.Which of the following is one example by which cancer cells (or tumors) can promote their own continual proliferation? Select any/all examples that apply.
A. Tumor cells signal surrounding stromal cells to release growth factors.
B. Cancer cells constitutively activate signaling pathways that lie downstream of growth factor receptors.
C. Cancer cells chronically stimulate the intrinsic apoptosis pathway.
D. Tumors encourage necrotic cell death so as to decrease pro-inflammatory signals.
E. Cancer cells decrease the expression levels of PTEN.
7.Necrotic cells can be tumor-promoting because: (select any/all answers that apply)
A. they release anti-inflammatory signaling molecules.
B. they express gain-of-function mutations in Beclin-1.
C. they release interleukins which then promote proliferation.
D. they recruit pro-inflammatory immune cells which then promote angiogenesis.
E. they release TGF.
8.Which of the following is one mechanism by which cancer cells (or tumors) can increase mutational rates and/or genomic instability? Select any/all examples that apply.
A. loss-of-function mutations in caretaker genes
B. aerobic glycolysis
C. autophagy
D. overexpression of E-cadherin
E. loss of telomeric DNA
9.Caspases: (select all answers that apply)

A. are activated by IAPs.
B. are proteases.
C. are part of the extrinsic apoptotic pathway but not the intrinsic apoptotic pathway.
D. inhibit Bcl-2.
E. destroy the nuclear lamina.

10Which of the following is closely monitored through cell cycle checkpoint pathways? Select any/all answers that apply.
A. cell growth
B. DNA replication
C. DNA damage
D. proper kinetochore attachment
E. proper spindle positioning

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