Correct option is A
Answer: A and C (option a)
Explanation
-uPA promotes invasion/metastasis by binding the cell-surface uPA receptor (uPAR) to focus proteolytic activity and trigger signaling for cell migration.
-A mutant uPA that cannot bind uPAR will not promote receptor-dependent invasion, so primary tumour formation (driven by other oncogenic events) can still occur while metastasis is reduced.
-A secreted (soluble) uPAR acts as a decoy that sequesters uPA and prevents uPA–uPAR interactions at the cell surface, so it reduces metastasis but does not necessarily block tumour formation.
Information Booster
-uPA–uPAR interaction localizes plasminogen activation to the cell surface, generating plasmin that degrades extracellular matrix and activates other proteases—key for invasion and metastasis.
-Decoy receptors or receptor-binding mutants commonly reduce invasive behaviour while leaving proliferation (tumour growth) largely unaffected unless the pathway also controls growth signals.
Additional Knowledge — why the other options are wrong
-B (mutant uPA that does not bind uPAR → enhanced tumour formation and metastasis): contradicts mechanism — loss of receptor binding should reduce invasion/metastasis, not enhance it.
-D (secreted uPAR reduces tumour formation as well as metastasis): unlikely because soluble uPAR blocks uPA-mediated invasion but typically does not eliminate primary tumour growth unless uPA–uPAR is also essential for proliferation in that model (not implied here).
