鈣池調控鈣離子流入（SOCE）是在非興奮性細胞中主要造成鈣離子進入細胞的機制，鈣離子也參與在調控血管新生訊息傳遞路徑。基質交互分子（STIM1）是位於內質網膜上的鈣離子感測蛋白，當內質網中儲存的鈣離子濃度降低時， STIM1會活化、聚集形成團簇、運輸到細胞膜附近，與細胞膜上鈣池調控鈣離子通道蛋白Orai1產生交互作用，進而啟動SOCE。在啟動SOCE過程，STIM1可直接重組微管的結構再移動至細胞膜附近，因此，微管的轉譯後修飾調控會影響微管的特性及功能，其中-微管蛋白離胺酸40進行乙醯化能夠穩固微管的結構。為了闡明STIM1在子宮頸癌惡性腫瘤的角色，我利用重度合併免疫缺失小鼠腫瘤移植活體模式以皮下注射方式打入STIM1過度表現以及STIM1抑制的子宮頸癌SiHa細胞株，STIM1過度表現的腫瘤有較大的體積並且周圍富含著血管，相反的，STIM1抑制的會延遲腫瘤的生長及血管生成，實驗結果暗示STIM1部份藉由血管新生促進腫瘤生長。血管內皮生長因子(VEGF-A)是由腫瘤細胞分泌促進血管新生主要的生長因子；並且利用酵素連結免疫吸附法(ELISA)檢測腫瘤細胞VEGF-A的分泌量，支持STIM1蛋白表現量的多寡會調節腫瘤細胞VEGF-A分泌的假設。接下來進一步使用組蛋白去乙醯酶6抑制劑A292與太平洋紫杉醇(paclitaxel, Taxol)試驗微管乙醯化對於STIM1活化過程的影響，組蛋白去乙醯酶6抑制劑A292增加-微管蛋白離胺酸40進行乙醯化，即使在表皮生長因果子刺激下，依然能夠抑制STIM1牽引至細胞膜；太平洋紫杉醇是已知能將微管乙醯化和促進-微管蛋白聚合作用的化學治療藥物，也會增加-微管蛋白乙醯化與遏止STIM1的運送。整體而言，我認為STIM1藉由調控血管新生促進子宮頸癌腫瘤生長，並且微管乙醯化能夠抑制STIM1運送至細胞膜附近，可提供予未來臨床應用。

Store-operated calcium entry (SOCE) is a major Ca2+ influx in non-excitable cells. Ca2+ is also a key regulator of signaling pathways in angiogenesis. Stromal interaction molecule 1 (STIM1) is an endoplasmic reticulum (ER)-localized Ca2+ sensor. In response to ER Ca2+ concentration depletion, STIM1 rearranges into punctate clusters, traffics to plasma membrane, and interacts with the Ca2+ release activated Ca2+ (CRAC) channel, Orai1, then triggers SOCE. STIM1 also directly reorganizes microtubules in the SOCE pathway. Post-translational modifications of microtubules regulate microtubule properties as well as microtubule-based cellular functions. Acetylation of -tubulin on lysine 40 is fairly common and can be found on stable microtubules in most cell types. To elucidate the role of STIM1 in cervical malignancy, I inoculated STIM1 overexpressed or knockdown cervical cancer SiHa cells in vivo by using tumor xenograft SCID mice model. STIM1 overexpression results in larger tumor mass with enriched tumor vessels. On contrast, STIM1 knockdown impedes tumor growth with less tumor vessels. These results indicate that STIM1 may promote tumor growth partly through angiogenesis. Vascular endothelial growth factor-A (VEGF-A) is the most growth factor produced by cancer cells that stimulates the growth of new blood vessels. The enzyme-linked immunosorbent assays (ELISA) for quantitative VEGF-A detections support the hypothesis that tumor STIM1 abundance would regulate VEGF-A secretion from cancer cells. I also test the effect of histone deacetylase 6 (HDAC6) inhibitor, A292, and paclitaxel (Taxol) on STIM1 activation. The HDAC6 inhibitor increases -tubulin acetylation and inhibits trafficking of STIM1 near plasma membrane even with epidermal growth factor stimulation. The well-known -tubulin polymerization chemotherapeutic agent, paclitaxel, also augments -tubulin acetylation and restrains trafficking of STIM1. Taken these data together, STIM1 can enhance cervical cancer growth partly by regulating tumor angiogenesis. Acetylation of microtubules by the HDAC6 inhibitor, A292, and paclitaxel abolish trafficking of STIM1 toward juxta-plasma membrane, providing a potential targeting to inhibit STIM1 activation.

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