Abstract
Gene mutation’s role in initiating carcinogenesis has been controversial, but it is consensually accepted that both carcinogenesis and cancer metastasis are gene-regulated processes. MTA1, a metastasis-associated protein, has been extensively researched, especially regarding its role in cancer metastasis. In this review, I try to elucidate MTA1’s role in both carcinogenesis and metastasis from a different angle. I propose that MTA1 is a stress response protein that is upregulated in various stress-related situations such as heat shock, hypoxia, and ironic radiation. Cancer cells are mostly living in a stressful environment of hypoxia, lack of nutrition, and immune reaction attacks. To cope with all these stresses, MTA1 expression is upregulated, plays a role of master regulator of gene expression, and helps cancer cells to survive and migrate out of their original dwelling.
Highlights
Metastasis is the primary cause of cancer-related death
IDH1 and IDH2 mutations are associated with better glioma patient prognosis [7,8,9], and Braf mutations are associated with better prognosis in acral lentiginous melanoma [10]
The stepwise carcinogenesis model was gradually accepted by the scientific field. This model asserts that an epithelial cell is malignantly transformed due to gene mutation, further proliferates to form atypical hyperplasia, progresses to in situ carcinoma, and with gene mutation accumulation, it breaks down the basement membrane separating the epithelium from the connective stroma
Summary
Metastasis is the primary cause of cancer-related death. In the past half century, paramount efforts have been made to elucidate the mechanisms involved in cancer metastasis, especially molecular mechanisms, with an aim to design. Wang State Key Lab for Cancer Biology, Department of Pathology, Xijing Hospital, Xi’an, China. The traditional view of carcinogenesis as a result of accumulated gene mutation faces increasing challenges [1,2,3,4,5] and evidence falsifying the somatic mutation theory (SMT) is emerging. Intensive cancer genome studies failed to reveal any specific gene mutation combinations as the cause of cancer. Increasing evidence shows that most high occurrence gene mutations in cancer cells are associated with better clinical outcomes, which means gene mutations lower cancer malignancy. IDH1 and IDH2 mutations are associated with better glioma patient prognosis [7,8,9], and Braf mutations are associated with better prognosis in acral lentiginous melanoma [10]
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