AbMole小課堂丨Gastrin-I（胃泌素），類器官高效培養(yǎng)的“明星分子”類器官作為一種新興的三維細胞培養(yǎng)模型，能夠高度模擬體內(nèi)器官的結(jié)構(gòu)和功能。在類器官培養(yǎng)過程中，小分子調(diào)節(jié)劑和細胞因子發(fā)揮著關(guān)鍵作用，它們之間的不同組合可用于培養(yǎng)多種類器官。Gastrin-I（胃泌素，AbMole，M9320）作為一種重要的膽囊收縮素2受體（CCK2R）的選擇性激動劑，對胃腸道、肝臟和多種腫瘤類器官的生長、發(fā)育及功能維持具有重要影響。Gastrin-I的作用機理Gastrin-I（胃泌素，AbMole，M9320）是一種多肽類生物活性分子，Gastrin-I通過與CCK2R結(jié)合，激活細胞內(nèi)信號通路，如提高細胞內(nèi)Ca2+濃度、促進磷酸肌醇生成和蛋白激酶C激活。此外，Gastrin-I還參與胃上皮細胞的增殖和分化過程，刺激胃泌酸腺區(qū)黏膜和十二指腸黏膜的DNA、RNA及蛋白質(zhì)合成，促進黏膜細胞的生長與增殖。Gastrin-I用于類器官的培養(yǎng)在胃類器官的培養(yǎng)過程中，Gastrin-I（胃泌素，AbMole，M9320）是培養(yǎng)基中的重要組分。研究表明，Gastrin-I能夠通過其受體激活下游信號通路，從而促進胃上皮細胞的增殖和分化。例如，在一項研究中，Gastrin-I被添加到3D胃類器官的培養(yǎng)基中，濃度為1nM，與其他生長因子如表皮生長因子（EGF）和成纖維細胞生長因子10（FGF10）協(xié)同作用，顯著提高了類器官的形成效率和生長速度ADDINEN.CITE<EndNote><Cite><Author>Chakrabarti</Author><Year>2020</Year><RecNum>466</RecNum><DisplayText><styleface="superscript">[1]</style></DisplayText><record><rec-number>466</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1752041398">466</key></foreign-keys><ref-typename="BookSection">5</ref-type><contributors><authors><author>Chakrabarti,Jayati</author><author>Zavros,Yana</author></authors><secondary-authors><author>Spence,JasonR.</author></secondary-authors></contributors><titles><title>Chapter2-GenerationanduseofgastricorganoidsforthestudyofHelicobacterpyloripathogenesis</title><secondary-title>MethodsinCellBiology</secondary-title></titles><pages>23-46</pages><volume>159</volume><keywords><keyword>Organoid</keyword><keyword>Gastricmetaplasia</keyword><keyword>Gastriccancer</keyword><keyword>Gastritis</keyword></keywords><dates><year>2020</year><pub-dates><date>2020/01/01/</date></pub-dates></dates><publisher>AcademicPress</publisher><isbn>0091-679X</isbn><urls><related-urls><url>/science/article/pii/S0091679X20300753</url></related-urls></urls><electronic-resource-num>/10.1016/bs.mcb.2020.04.011</electronic-resource-num></record></Cite></EndNote>[1]。這種培養(yǎng)體系不僅能夠模擬胃組織的生理結(jié)構(gòu)，還為研究胃腸道疾病提供了理想的模型ADDINEN.CITE<EndNote><Cite><Author>Chakrabarti</Author><Year>2020</Year><RecNum>466</RecNum><DisplayText><styleface="superscript">[1]</style></DisplayText><record><rec-number>466</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1752041398">466</key></foreign-keys><ref-typename="BookSection">5</ref-type><contributors><authors><author>Chakrabarti,Jayati</author><author>Zavros,Yana</author></authors><secondary-authors><author>Spence,JasonR.</author></secondary-authors></contributors><titles><title>Chapter2-GenerationanduseofgastricorganoidsforthestudyofHelicobacterpyloripathogenesis</title><secondary-title>MethodsinCellBiology</secondary-title></titles><pages>23-46</pages><volume>159</volume><keywords><keyword>Organoid</keyword><keyword>Gastricmetaplasia</keyword><keyword>Gastriccancer</keyword><keyword>Gastritis</keyword></keywords><dates><year>2020</year><pub-dates><date>2020/01/01/</date></pub-dates></dates><publisher>AcademicPress</publisher><isbn>0091-679X</isbn><urls><related-urls><url>/science/article/pii/S0091679X20300753</url></related-urls></urls><electronic-resource-num>/10.1016/bs.mcb.2020.04.011</electronic-resource-num></record></Cite></EndNote>[1]。圖SEQ圖\*ARABIC1.胃和腸道類器官的構(gòu)建ADDINEN.CITEADDINEN.CITE.DATA[2]在小腸和結(jié)腸類器官培養(yǎng)中，Gastrin-I同樣具有重要意義。Gastrin-I（胃泌素，AbMole，M9320）能夠促進結(jié)腸上皮細胞的增殖和分化，維持結(jié)腸類器官的穩(wěn)定性和功能性。在結(jié)腸類器官的培養(yǎng)基中，Gastrin-I通常與TGF-β抑制劑如A83-01（AbMole，M5037）、LY2157299（AbMole，M1980）和p38MAPK抑制劑如SB202190（AbMole，M2062）協(xié)同作用，以支持結(jié)腸干細胞的擴增和分化ADDINEN.CITE<EndNote><Cite><Author>Barbáchano</Author><Year>2021</Year><RecNum>465</RecNum><DisplayText><styleface="superscript">[3]</style></DisplayText><record><rec-number>465</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1752040927">465</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Barbáchano,Antonio</author><author>Fernández-Barral,Asunción</author><author>Bustamante-Madrid,Pilar</author><author>Prieto,Isabel</author><author>Rodríguez-Salas,Nuria</author><author>Larriba,MaríaJesús</author><author>Mu?oz,Alberto</author></authors></contributors><titles><title>OrganoidsandColorectalCancer</title></titles><pages>2657</pages><volume>13</volume><number>11</number><dates><year>2021</year></dates><isbn>2072-6694</isbn><accession-num>doi:10.3390/cancers13112657</accession-num><urls><related-urls><url>/2072-6694/13/11/2657</url></related-urls></urls></record></Cite></EndNote>[3]。此外，Gastrin-I在小腸類器官的代謝功能中也具有重要作用，它能夠調(diào)節(jié)小腸上皮細胞的吸收功能，促進營養(yǎng)物質(zhì)的吸收和轉(zhuǎn)運。這種調(diào)節(jié)作用對于維持小腸類器官的生理功能和穩(wěn)定性至關(guān)重要ADDINEN.CITE<EndNote><Cite><Author>Barbáchano</Author><Year>2021</Year><RecNum>465</RecNum><DisplayText><styleface="superscript">[3]</style></DisplayText><record><rec-number>465</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1752040927">465</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Barbáchano,Antonio</author><author>Fernández-Barral,Asunción</author><author>Bustamante-Madrid,Pilar</author><author>Prieto,Isabel</author><author>Rodríguez-Salas,Nuria</author><author>Larriba,MaríaJesús</author><author>Mu?oz,Alberto</author></authors></contributors><titles><title>OrganoidsandColorectalCancer</title></titles><pages>2657</pages><volume>13</volume><number>11</number><dates><year>2021</year></dates><isbn>2072-6694</isbn><accession-num>doi:10.3390/cancers13112657</accession-num><urls><related-urls><url>/2072-6694/13/11/2657</url></related-urls></urls></record></Cite></EndNote>[3]。Gastrin-I（胃泌素，AbMole，M9320）在肝臟類器官培養(yǎng)中也是必不可少的成分之一。研究表明，Gastrin-I能夠通過激活下游信號通路，從而促進肝細胞的增殖和分化。在肝臟類器官的培養(yǎng)基中，Gastrin-I通常與其他生長因子如EGF（AbMole，M10016）、FGF10（AbMole，M10353）和HGF（AbMole，M10352）協(xié)同作用，以支持肝臟干細胞的擴增和分化。例如，一項研究中提到，在肝臟類器官的培養(yǎng)基中添加10nM的重組人Gastrin-I，能夠顯著提高類器官的形成效率和生長速度ADDINEN.CITEADDINEN.CITE.DATA[4]。Gastrin-I（胃泌素，AbMole，M9320）還被廣泛用于多種腫瘤類器官的培養(yǎng)，包括胃癌、結(jié)腸癌、胰腺癌和肝癌等。為腫瘤類器官在疾病研究和藥物篩選中的應(yīng)用提供了重要的支持。范例詳解

上海交通大學、吉林大學的研究團隊探索了胰腺導管腺癌（PDAC）在Gemcitabine耐藥性發(fā)展過程中的動態(tài)表觀遺傳學變化，特別是超級增強子及其調(diào)控效應(yīng)。研究使用了Gemcitabine耐藥（Gem-R）的PDAC細胞系，并構(gòu)建了類器官模型。實驗人員還進行了高通量的表觀基因組、增強子連接組和轉(zhuǎn)錄組分析。研究發(fā)現(xiàn)，在從Gemcitabine敏感到耐藥的PDAC細胞轉(zhuǎn)變過程中，表觀遺傳景觀和基因組結(jié)構(gòu)發(fā)生了顯著變化。特別是超級增強子的激活狀態(tài)表現(xiàn)出極大的可塑性，許多順式元件在耐藥細胞中被去激活。此外，研究還確定了NDRG1超級增強子（NDRG1-SE）是Gemcitabine耐藥中一個關(guān)鍵的調(diào)控因子，NDRG1-SE的關(guān)閉誘導了WNT/β-catenin信號通路的激活，從而賦予了細胞對Gemcitabine的耐藥ADDINEN.CITE<EndNote><Cite><Author>Wei</Author><Year>2024</Year><RecNum>467</RecNum><DisplayText><styleface="superscript">[5]</style></DisplayText><record><rec-number>467</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1752042292">467</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Wei,Dianhui</author><author>Yuan,Lili</author><author>Xu,Xiaoli</author><author>Wu,Chengsi</author><author>Huang,Yiwen</author><author>Zhang,Lili</author><author>Zhang,Jilong</author><author>Jing,Tiantian</author><author>Liu,Yizhen</author><author>Wang,Boshi</author></authors></contributors><titles><title>Exploringepigeneticdynamicsunveilsasuper-enhancer-mediatedNDRG1-β-cateninaxisinmodulatinggemcitabineresistanceinpancreaticcancer</title><secondary-title>CancerLetters</secondary-title></titles><periodical><full-title>CancerLett</full-title><abbr-1>Cancerletters</abbr-1></periodical><pages>217284</pages><volume>605</volume><keywords><keyword>Super-enhancer</keyword><keyword>Dynamicepigeneticlandscape</keyword><keyword>Pancreaticductaladenocarcinoma(PDAC)</keyword><keyword>Gemcitabineresistance</keyword></keywords><dates><year>2024</year><pub-dates><date>2024/11/28/</date></pub-dates></dates><isbn>0304-3835</isbn><urls><related-urls><url>/science/article/pii/S0304383524006797</url></related-urls></urls><electronic-resource-num>/10.1016/j.canlet.2024.217284</electronic-resource-num></record></Cite></EndNote>[5]。在上述研究中，實驗人員使用了由AbMole提供的多個產(chǎn)品：GastrinI（胃泌素，AbMole，M9320）、Forskolin（AbMole，M2191）、Y-27632（AbMole，M1817）、A83-01（AbMole，M5037）、Dexamethasone（AbMole，M2176）、ProstaglandinE2（AbMole，M5929）、Nicotinamide（AbMole，M4896），并用于PDAC類器官的培養(yǎng)ADDINEN.CITE<EndNote><Cite><Author>Wei</Author><Year>2024</Year><RecNum>468</RecNum><DisplayText><styleface="superscript">[5]</style></DisplayText><record><rec-number>468</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1752043368">468</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Wei,Dianhui</author><author>Yuan,Lili</author><author>Xu,Xiaoli</author><author>Wu,Chengsi</author><author>Huang,Yiwen</author><author>Zhang,Lili</author><author>Zhang,Jilong</author><author>Jing,Tiantian</author><author>Liu,Yizhen</author><author>Wang,Boshi</author></authors></contributors><titles><title>Exploringepigeneticdynamicsunveilsasuper-enhancer-mediatedNDRG1-β-cateninaxisinmodulatinggemcitabineresistanceinpancreaticcancer</title><secondary-title>CancerLetters</secondary-title></titles><periodical><full-title>CancerLett</full-title><abbr-1>Cancerletters</abbr-1></periodical><pages>217284</pages><volume>605</volume><keywords><keyword>Super-enhancer</keyword><keyword>Dynamicepigeneticlandscape</keyword><keyword>Pancreaticductaladenocarcinoma(PDAC)</keyword><keyword>Gemcitabineresistance</keyword></keywords><dates><year>2024</year><pub-dates><date>2024/11/28/</date></pub-dates></dates><isbn>0304-3835</isbn><urls><related-urls><url>/science/article/pii/S0304383524006797</url></related-urls></urls><electronic-resource-num>/10.1016/j.canlet.2024.217284</electronic-resource-num></record></Cite></EndNote>[5]。圖SEQ圖\*ARABIC2.InductionofChemoresistancetoGemcitabinebyNDRG1Super-EnhancerDeactivationADDINEN.CITE<EndNote><Cite><Author>Wei</Author><Year>2024</Year><RecNum>468</RecNum><DisplayText><styleface="superscript">[5]</style></DisplayText><record><rec-number>468</rec-number><foreign-keys><keyapp="EN"db-id="f2td9w00a22awteprfrp9vaup9d9zwa9tdfr"timestamp="1752043368">468</key></foreign-keys><ref-typename="JournalArticle">17</ref-type><contributors><authors><author>Wei,Dianhui</author><author>Yuan,Lili</author><author>Xu,Xiaoli</author><author>Wu,Chengsi</author><author>Huang,Yiwen</author><author>Zhang,Lili</author><author>Zhang,Jilong</author><author>Jing,Tiantian</author><author>Liu,Yizhen</author><author>Wang,Boshi</author></authors></contributors><titles><title>Exploringepigeneticdynamicsunveilsasuper-enhancer-mediatedNDRG1-β-cateninaxisinmodulatinggemcitabineresistanceinpancreaticcancer</title><secondary-title>CancerLetters</secondary-title></titles><periodical><full-title>CancerLett</full-title><abbr-1>Cancerletters</abbr-1></periodical><pages>217284</pages><volume>605</volume><keywords><keyword>Super-enhancer</keyword><keyword>Dynamicepigeneticlandscape</keyword><keyword>Pancreaticductaladenocarcinoma(PDAC)</keyword><keyword>Gemcitabineresistance</keyword></keywords><dates><year>2024</year><pub-dates><date>2