Abstract
Clinical studies and cancer cell models emphasize the importance of targeting therapies for oral cancer. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is highly expressed in cancer, and is a selective killing ligand for oral cancer. Signaling proteins in the wingless-type mouse mammary tumor virus (MMTV) integration site family (Wnt), Sonic hedgehog (SHH), and transforming growth factor β (TGFβ) pathways may regulate cell proliferation, migration, and apoptosis. Accordingly, the genes encoding these signaling proteins are potential targets for oral cancer therapy. In this review, we focus on recent advances in targeting therapies for oral cancer and discuss the gene targets within TRAIL, Wnt, SHH, and TGFβ signaling for oral cancer therapies. Oncogenic microRNAs (miRNAs) and tumor suppressor miRNAs targeting the genes encoding these signaling proteins are summarized, and the interactions between Wnt, SHH, TGFβ, and miRNAs are interpreted. With suitable combination treatments, synergistic effects are expected to improve targeting therapies for oral cancer.
Highlights
The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), referred to as the tumor necrosis factor superfamily, member 10 (TNFSF10), is an apoptosis-inducible cytokine [1]
In OSCC cells, the non-canonical wingless-type MMTV integration site family (Wnt)/Ca2+/protein kinase C (PKC) pathway is activated via the Wnt family member 5A (WNT5A), enhancing migration and invasion [47]
transforming growth factor β (TGFβ)-signaling proteins were overexpressed in OSCC, and have become potential targets for oral cancer therapies
Summary
The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), referred to as the tumor necrosis factor (ligand) superfamily, member 10 (TNFSF10), is an apoptosis-inducible cytokine [1]. TRAIL may crosstalk to transforming growth factor β (TGFβ; TGFB1) in disease progression and apoptosis. TRAIL-induced death-inducing signaling complex (DISC) formation for apoptosis was inhibited in TGFβ-treated human breast epithelial cells [5]. TRAIL and TGFβ may crosstalk to regulate migration and apoptosis. TGFβ, SHH, and wingless-type MMTV integration site family (Wnt) crosstalk to regulate mesenchymal transition (EMT) [8] in tumor progression [9]. These signalings are potential targets for cancer therapy. The following sections aim to summarize updated literature on the roles of TRAIL, TGFβ, SHH, Wnt, and miRNAs as potential targets for oral cancer therapy
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