Abstract
Human papillomaviruses (HPVs) and the Epstein–Barr virus (EBV) are the most common oncoviruses, contributing to approximately 10%–15% of all malignancies. Oncoproteins of high-risk HPVs (E5 and E6/E7), as well as EBV (LMP1, LMP2A and EBNA1), play a principal role in the onset and progression of several human carcinomas, including head and neck, cervical and colorectal. Oncoproteins of high-risk HPVs and EBV can cooperate to initiate and/or enhance epithelial-mesenchymal transition (EMT) events, which represents one of the hallmarks of cancer progression and metastasis. Although the role of these oncoviruses in several cancers is well established, their role in the pathogenesis of colorectal cancer is still nascent. This review presents an overview of the most recent advances related to the presence and role of high-risk HPVs and EBV in colorectal cancer, with an emphasis on their cooperation in colorectal carcinogenesis.
Highlights
Colorectal cancer is one of the most prevalent types of cancers worldwide [1] that is known to progress gradually over long periods of time [2]
We reported that E6/E7 oncoproteins of high-risk human papillomaviruses (HPVs) type 16 cooperate with the ErbB-2 receptor to provoke cellular transformation of normal epithelial cells [63]
While it is important to state that the role of E5 oncoprotein in these malignancies still lies nascent, it has been reported that E5 of high-risk HPVs can affect cell alteration and lead to oncogenesis via its interaction with EGF-R1 pathways, MAP kinase and
Summary
Colorectal cancer is one of the most prevalent types of cancers worldwide [1] that is known to progress gradually over long periods of time [2]. The E2 gene is a negative regulator of the E6/E7 oncoproteins that bind to tumor suppressor molecules like p53 and pRB respectively, disrupting their tumor suppressing activity [60] This phenomenon is known to mark oncogenesis that further leads to genomic instability and cellular transformation [61,62]; indicating mechanism of HPV-induced colorectal carcinogenesis. We reported that E6/E7 oncoproteins of high-risk HPV type 16 cooperate with the ErbB-2 receptor to provoke cellular transformation of normal epithelial cells [63]. While it is important to state that the role of E5 oncoprotein in these malignancies still lies nascent, it has been reported that E5 of high-risk HPVs can affect cell alteration and lead to oncogenesis via its interaction with EGF-R1 pathways, MAP kinase and PI3K-Akt, as well as pro-apoptotic proteins [70,71,72]. The role of HPV oncoproteins in cancer, in colorectal cancer is not fully elucidated
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