研究人員首次揭示了性激素受體（如GRPR）在癌癥轉移中的重要作用，并闡明了其背后的分子機制。

如今，癌癥已成為威脅人類健康的重大殺手之一，而性激素在癌癥發生和發展中的作用更是引起了廣泛關注。近年來，隨著精準醫療的興起，科學家們逐漸意識到，不同性別、不同年齡段的癌癥患者在治療反應和疾病進展上存在著顯著差異，這一發現引發了科學家們對性激素如何影響癌癥行為的深入探討。

近日，一篇發表在國際雜志Nature上題為“Targeting GRPR for sex hormone-dependent cancer after loss of E-cadherin”的研究報告中，來自巴黎文理研究大學等機構的科學家們通過研究揭示了性激素受體與癌癥轉移之間的關系，特別是GRPR（胃泌素釋放肽受體）在其中的關鍵作用，相關研究結果或為癌癥治療提供了新的思路。

這項研究中，研究人員旨在揭示性激素如何通過影響特定受體的表達進而調控癌癥的轉移能力，通過深入分析E-鈣粘蛋白（E-cadherin）在性激素信號傳導中的作用，他們發現了一條連接性激素與癌癥轉移的新途徑，這一發現不僅加深了我們對癌癥轉移機制的理解，更為開發新的抗癌療法提供了理論依據和實驗基礎。

研究人員以小鼠黑色素瘤模型為主要實驗對象，同時結合人類黑色素瘤和乳腺癌樣本進行分析，實驗中采用了基因編輯技術（如CRISPR-Cas9）、細胞培養、動物模型構建、RNA測序、ChIP-seq等多種技術手段，對E-鈣粘蛋白、GRPR、ERα（雌激素受體α）等關鍵分子的表達和功能進行了深入研究。

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E-鈣粘蛋白是雌激素介導的癌癥反應的關鍵樞紐，其在黑色素瘤轉移中具有性別依賴效應

首先他們通過構建條件性敲除E-鈣粘蛋白的小鼠黑色素瘤模型，觀察了E-鈣粘蛋白缺失對腫瘤轉移的影響；隨后利用RNA測序和ChIP-seq技術揭示了E-鈣粘蛋白缺失后腫瘤細胞內基因表達譜的變化，特別是GRPR和ERα的上調表達。為了進一步驗證這些發現，研究者們還在人類黑色素瘤和乳腺癌樣本中進行了相關分析并探討了性激素對這些樣本中GRPR表達的影響。

研究結果表明，E-鈣粘蛋白的缺失會導致B-catenin信號通路的激活進而上調ERα和GRPR的表達。GRPR的激活則會通過Gaq/11-PKC-YAP1信號軸來促進腫瘤細胞的侵襲和轉移。此外，性激素（特別是雌激素）能通過調控ERα進一步影響GRPR的表達和活性，這些發現表明，性激素信號通路與癌癥轉移之間存在密切聯系，而GRPR則可能成為抗癌治療的新靶點。

這項研究中，研究人員首次揭示了性激素受體（如GRPR）在癌癥轉移中的重要作用，并闡明了其背后的分子機制。這一發現不僅挑戰了我們對癌癥轉移的傳統認識，更為開發針對性激素受體的抗癌療法提供了新思路。未來，研究者們還將進一步探索GRPR抑制劑在癌癥治療中的潛力從而為患者帶來更加有效和安全的治療方案。