Most of cancer cell lines have mutation of tumor suppressor genes which you ask. PTEN is well-known to increase the susceptibility to the genetic mutation or epigenetic alteration to induce Ras signal activation. Rb is responsible for a major G1 checkpoint in the cell cycle regulation. Further, Rb is known to the cause of retinoblastoma. Finally, p53 is the "gatekeeper" of DNA mismatch mutation and the lack of p53 results in the genetic instability. Of note, HCT-116 exceptionally expresses p53 and the knockdown of p53 increases the expression level of CD44, one of the cancer stem cell markers. 

Thank you!

I've read somewhere that the mutations of p53 and  PTEN has an effect on cells' membrane, cells' surface morphology, it causes somekind of membrane folding, membrane extensions like microvilli, filopodia which may lead to the invasive behaviour (in humans GBM cancer cells), does it have to do something with the DNA mismatch?

We have HCT116 p53 wildtype and knockout cells. I haven't compared these two cell lines. But in my experience, p53 knocoout HCT116 cells are more sensitive to genotoxic stress and less viable (never detected metabolic parameters). Maybe you can take a look at this paper to find some clue.

Article Tumor suppressor p53 cooperates with SIRT6 to regulate gluco...

Thank you!

Have you done some research and could you share something on PTEN and Rb too?