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Migration and invasion of tumor cells are essential prerequisites for the formation of metastasis in malignant diseases. Previously, we have reported that CC chemokine receptor 7 (CCR7) regulates the mobility of squamous cell carcinoma of head and neck (SCCHN) cells through several pathways, such as integrin and cdc42. In this study, we investigated the connection between CCR7 and mitogen-activated protein kinase (MAPK) family members, and their influence on cell invasion and migration in metastatic SCCHN cells. Western blotting, immunostaining and fluorescence microcopy were used to detect the protein expression and distribution of MAPKs, and the Migration assay, Matrigel invasion assay and wound-healing assay to detect the role of MAPKs in CCR7 regulating cell mobility. To analyze the correlation between CCR7 and MAPK activity and clinicopathological factors immunohistochemical staining was emplyed. The results showed stimulation of CCL19 and the activation of CCR7 could induce ERK1/2 and JNK phosphorylation, while it had no efect on p38. After activation, ERK1/2 and JNK promoted E-cadherin low expression and Vimentin high expression. The MAPK pathway not only mediated CCR7 induced cell migration, but also mediated invasion speed. The immunohistochemistry results showed that CCR7 was correlated with the phosphorylation of ERK1/2 and JNK in SCCHN, and these molecules were all associated with lymph node metastasis. Therefore, our study demonstrates that MAPK members (ERK1/2 and JNK) play a key role in CCR7 regulating SCCHN metastasis.

BackgroundThe large defects resulting from head and neck tumour surgeries present a reconstructive challenge to surgeons. Although numerous methods can be used, they all have their own limitations. In this paper, we present our experience with cervicofacial and cervicothoracic rotation flaps to help expand the awareness and application of this useful system of flaps.MethodsTwenty-one consecutive patients who underwent repair of a variety of defects of the head and neck with cervicofacial or cervicothoracic flaps in our hospital from 2006 to 2009 were retrospectively analysed. Statistics pertaining to the patients' clinical factors were gathered.ResultsCheek neoplasms are the most common indication for cervicofacial and cervicothoracic rotation flaps, followed by parotid tumours. Among the 12 patients with medical comorbidities, the most common was hypertension. Defects ranging from 1.5 cm × 1.5 cm to 7 cm × 6 cm were reconstructed by cervicofacial flap, and defects from 3 cm × 2 cm to 16 cm × 7 cm were reconstructed by cervicothoracic flap. The two flaps also exhibited versatility in these reconstructions. When combined with the pectoralis major myocutaneous flap, the cervicothoracic flap could repair through-and-through cheek defects, and in combination with a temporalis myofacial flap, the cervicofacial flap was able to cover orbital defects. Additionally, 95% patients were satisfied with their resulting contour results.ConclusionsCervicofacial and cervicothoracic flaps provide a technically simple, reliable, safe, efficient and cosmetic means to reconstruct defects of the head and neck.

Squamous cell carcinoma of the head and neck (SCCHN) frequently involves metastasis at diagnosis. Our previous research has demonstrated that CCR7 plays a key role in regulating SCCHN metastasis, and this process involves several molecules, such as PI3K/cdc42, pyk2, and Src. In this study, the goals are to identify whether JAK2/STAT3 also participates in CCR7's signal network, its relationship with other signal pathways, and its role in SCCHN cell invasion and migration. The results showed that stimulation of CCL19 could induce JAK2/STAT3 phosphorylation, which can be blocked by Src and pyk2 inhibitors. After activation, STAT3 was able to promote low expression of E-cadherin and had no effect on vimentin. This JAk2/STAT3 pathway not only mediated CCR7-induced cell migration but also mediated invasion speed. The immunohistochemistry results also showed that the phosphorylation of STAT3 was correlated with CCR7 expression in SCCHN, and CCR7 and STAT3 phosphorylation were all associated with lymph node metastasis. In conclusion, JAk2/STAT3 plays a key role in CCR7 regulating SCCHN metastasis.