Recent advances in various treatment modalities, including targeted therapies, combination therapies, and immunotherapies, have improved the prognosis for many types of cancer. However, cancer treatments often provide a good initial response but ultimately lose their efficacy during disease progression, or the tumour may not even initially respond to treatment. The reasons behind these are typically the high mutation burden of tumours or the acquisition of resistance to treatment by cancer cells. Further research is essential to better understand the mechanisms of acquired resistance and to elucidate the molecular events that lead to cancer invasion and metastatic dissemination. It is also important to identify new target molecules for cancer treatments and develop biomarkers for clinical use.

Specific actin structures and dynamics are tightly controlled and essential for most cellular functions and homeostasis. The formin protein family comprises 15 members, which are important regulators of the actin cytoskeleton and participate in various developmental and homeostatic cellular processes, including cell division, organelle trafficking, actin-dependent cell signalling, and cell migration. Altered functions of formins are linked to various cancers, but there is a need for cancer-specific studies.

This thesis analyses the expression of formins FHOD1, DAAM1, and INF2 along with their functional roles in two types of cancer: cutaneous melanoma and HER2-positive breast cancer. FHOD1 expression was mainly strong in cutaneous melanoma and cultured melanoma cells. The reduction of FHOD1 affected the ability of melanoma cells to attach, migrate, and proliferate, and an in vivo experiment showed attenuation of tumour growth. In HER2-positive breast cancer, the expression levels of DAAM1, FHOD1, and INF2 correlated with outcomes and were associated with HER2/ERBB2 expression. The results revealed FHOD1 and INF2 as downstream effectors of HER2 in the PI3K and MAPK pathways. Additionally, DAAM1 was shown to function downstream of HER2 but independently of the PI3K and MAPK pathways. As these formins are involved in regulating critical cancer-related pathways, they could be considered candidates for future cancer treatments.