Methylprednisolone acetate, sold under the brand names Depo-Medrol among others, is a synthetic glucocorticoid corticosteroid and a corticosteroid ester—specifically the C21 acetate ester of methylprednisolone—which is used in clinical and veterinary medicine. It has been formulated as an aqueous suspension for intramuscular, intra-articular, soft tissue, and intralesional injection alone and in combination with lidocaine, a local anesthetic. Methylprednisolone acetate was previously suspended with polyethylene glycol but is no longer formulated with this excipient due to concerns about possible toxicity. Depo methylprednisolone acetate is a depot injection and is absorbed slowly with a duration of weeks to months with a single intramuscular injection. See also
List of corticosteroid esters § Methylprednisolone esters


== References ==
The N-terminal LXCXE motif of the LT protein has been shown to interact with known oncogene Rb and is conserved in other cancer-causing viruses. Studies suggest that LT may also preserve cell proliferation signals such as c-Myc and cyclin E and cause DNA injury to the p53 tumor suppressor.Meanwhile, sT has been shown to induce cell proliferation through hyper-phosphorylation of the translation initiator 4EBP1 as well as inhibition of a ubiquitin ligase complex responsible for degradation of cellular proliferation signals. sT also contains a region known as the LT stabilization domain (LSD), which potentiates the LT proteins oncogenic function. Unlike LT, MCC samples have been identified that express sT alone, and sT expression in fibroblasts has been shown to cause MCC phenotype development. UV light
About 20% of MCC tumors are MCV negative. In contrast to MCV-induced MCC, these tumors tend to have much higher mutational burdens with mutational signatures characteristic of UV damage. Genes frequently mutated in MCV-negative MCC include p53 and Rb, among others. The link between MCC and UV exposure has been demonstrated through various epidemiological studies indicating a higher incidence of MCC in fair-skinned people in areas of high UV exposure, as well as among those receiving UV phototherapy. The typical distribution of MCC in sun-exposed regions and its co-occurrence with other skin cancers also indicate that UV exposure is a contributing factor to MCC development. It is unclear whether this is through direct mutational impact, immune down-regulation, or some combination of the two.