HCT116 cells are homozygous for the (T)11 shortening which is the cause of the delat5-7 variant. These cells carry T10+T9 alleles.
Of course, the problem here is that you're dealing with a MSI cell line, that will accumulate more mutations during culturing. So HCT116 cells in one lab might not be identical to HCT116 cells in a different lab.
While the most common mutation for PolyN in MSI cells is shortenings, they can also undergo expansions, and some of them can be selected.
If you want to check whether there is a proportion of HCT116 with the wild-type T11 allele, one possibility would be subculturing and analyzing single-cell clones, always keeping in mind the inherent instability of the polyN sequences in these cells.
The Seltarbase website cites 2 papers and indicates biallelic mutation as in HCT116 Sergio described, with a high mutation frequency reported in both MSI-High cell lines and tumours. I agree that there may be further mutations with passaging in different labs.
If you can access or produce antibodies to the normal MRE11 protein C-terminus then these can be used to immunoprecipitate or western blot any normal protein compared with non mutated MSS controls. N-terminus Abs can demonstrate both the full length and truncated mutant proteins by this method (as in ref below).