淋巴結轉移或遠處轉移對頭頸部鱗狀細胞癌（HNSCC）的影響導致臨床的不良預後。調節癌症遷移和侵襲的機制在HNSCC中扮演重要作用。我們已經確定miR-455-5p與淋巴結轉移和臨床上腫瘤具有侵犯特徵(如淋巴結莢膜外侵犯)有關，導致口腔鱗狀細胞癌（OSCC）的不良預後。miR-455-5p誘導上皮間質轉化（EMT）並促進口腔癌細胞的遷移和侵襲。我們還確認了一個新的生物標記，PDZK1IP1 （MAP17），它為miR-455-5p的下游目標基因並與HNSCC的上皮分化有關。抑制PDZK1IP1的表現導致OSCC的遷移、轉移、EMT及增加轉化生長因子β（TGF-β）細胞訊號。此外，過度表達miR-455-5p或抑制PDZK1IP1促進OSCC的集體細胞遷移。TCGA和NCKU-OrCA-40TN的資料庫顯示，miR-455-5p與部分上皮間質轉化分數(partial EMT score)呈正相關，而PDZK1IP1與其則呈負相關。具有臨床侵犯特徵的患者PDZK1IP1表現量較低，partial EMT score較高。在這兩個資料庫中，partial EMT score可能是預測生存結果的標誌。在臨床患者樣本中，較高的miR-455-5p表現與高的vimentin和低的MAP17 H-score相關。表現高MAP17的患者具有更好的無復發生存比率。這些結果表明，miR-455-5p抑制PDZK1IP1的表現並促進OSCC疾病惡化。miR-455-5p和PDZK1IP1可能是重要的生物標誌物，並參與調節OSCC中的部分EMT。此外，我們已經證明MAP17可以通過外泌體分泌到微環境中，並探討了PDZK1IP1和TCGA頭頸癌數據庫中免疫相關分子之間的關聯。這些發現顯示，miR-455-5p和PDZK1IP1可能對HNSCC的免疫治療具有潛在的意義，並值得未來進一步研究。

Metastasis to lymph node or distant sites contribute to poor outcomes in head and neck squamous cell carcinoma (HNSCC). The mechanism that regulates cancer migration and invasion plays an important role in HNSCC. We have identified that miR-455-5p is associated with lymph node metastases and clinical invasion features, leading to poor outcomes in oral squamous cell carcinoma (OSCC). MiR-455-5p promotes oral cancer cell migration and invasion and induces epithelial to mesenchymal transition (EMT). We have also identified a novel biomarker, PDZK1IP1 (MAP17), which is targeted by miR-455-5p and associated with epithelial differentiation in HNSCC. PDZK1IP1 knockdown leads to migration, metastasis, EMT, and increased transforming growth factor beta (TGF-β) signaling in OSCC. Additionally, miR-455-5p overexpression and suppressed PDZK1IP1 promote collective cell migration in OSCC. Databases of TCGA and NCKU-OrCA-40TN have shown that miR-455-5p is positively correlated with the partial EMT score, whereas PDZK1IP1 has a negative correlation. Patients with clinical invasion features have lower PDZK1IP1 expression levels and higher partial EMT scores. The partial EMT score could be a predictive marker for survival outcomes in these two databases. In clinical patient samples, higher miR-455-5p expression is associated with high vimentin and low MAP17 H-score. Patients with high MAP17 expression have better recurrence-free survival and overall survival. These results suggest that miR-455-5p suppresses PDZK1IP1 expression and mediates OSCC progression. MiR-455-5p and PDZK1IP1 may be important biomarkers and participate in regulating partial EMT in OSCC. Furthermore, we have demonstrated that MAP17 can be secreted into the microenvironment through exosomes and have explored the association between PDZK1IP1 and immune molecules in TCGA head and neck datasets. These findings suggest that miR-455-5p and PDZK1IP1 may have potential implications for immunotherapy in HNSCC and warrant further investigation in the future.

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