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MK was shown to enhance the metastasis of Lewis lung carcinoma APY29 and promote cell migration/cell invasiveness [18] and [19]. MK is shown to play an important role in cell transformation, growth, survival, migration, invasiveness and angiogenesis, and becomes a promising target for anticancer therapy against the growth and spread of solid tumors [15], [16], [19], [21], [30] and [37]. “Constitutive expression of MK in responsive cells supports its role as a “tumor growth factor” and a positive regulator of tumor angiogenesis” [37]. Elucidating the molecular mechanisms of MK action in tumorgenesis and tumor angiogenesis may lead to the identification of novel targets for tumor therapy [15], [16] and [37].
We showed here that MK also physically associated with both TSPAN1 and integrin-α6β1 in turn inducing tyrosine phosphorylation of FAK, Stat1α and paxillin in HNSCC cells. Growth factors (e.g. MK) secreted by either host or tumor cells play a major role in tumor cell progression, stimulate cell migration and modulate the expression of MMP that are involved in tumor cell invasion and metastasis [1], [13], [17], [24], [25], [26], [27], [28] and [29]. We then observed that MK induced RNA and protein levels of MMP-2 and MMP-26 in HNSCC cells, whose expression was dramatically decreased by RNAi silencing of TSPAN1, Integrin-β1, FAK or Stat1α. The up-regulation of MMP-2 expression was reported during EMT in SCC cells [17], [24] and [29]. Thus, the major finding of this study is a novel MK-triggered signaling mechanism that implicated in migration and invasiveness of HNSCC cells.