股票在线配资开户引用格式：APA StyleHE

胃癌作为全球高发且预后不良的恶性肿瘤，一直是医学研究的重点领域。近两年来，《Oncology Research》发表了多篇聚焦胃癌的创新性研究，涵盖了分子机制、免疫治疗、新型靶点及治疗策略等多个方面。这些研究不仅深化了我们对胃癌发生发展机制的理解，也为临床诊断和精准治疗提供了新的思路和潜在靶点。本文合辑将为您呈现胃癌研究的最新进展，助力推动胃癌的科学研究与临床应用。

精选导读

Immunotherapy in gastric cancer—A systematic review

胃癌中的免疫治疗——系统综述

MARTA SANTOS, DIANA MARTINS, FERNANDO MENDES

展开剩余97%

Graphic Abstract

胃癌是全球第五大常见癌症和第四大致死癌症。近年来，免疫治疗作为一种新兴的治疗策略，在克服传统治疗局限性的同时，有望改善胃癌患者的临床结局。本系统综述总结了当前胃癌免疫治疗的研究进展，涵盖了过继性细胞治疗（ACT）、癌症疫苗和免疫检查点抑制剂（ICI）等主要治疗手段。研究通过筛选PubMed中236项相关研究，发现免疫检查点抑制剂，尤其是帕博利珠单抗（pembrolizumab），在改善总生存期（OS）、无进展生存期（PFS）及客观缓解率方面显示出良好的治疗潜力。安全性分析表明，免疫治疗总体耐受性良好，副作用可控。然而，仍需进一步探索肿瘤耐药机制并寻找有效的预测性生物标志物，以优化个体化治疗策略。

引用格式：

APA Style

SANTOS, M., MARTINS, D., MENDES, F. (2025). Immunotherapy in gastric cancer—A systematic review. Oncology Research, 33(2), 263–281. https://doi.org/10.32604/or.2024.052207

Vancouver Style

SANTOS M, MARTINS D, MENDES F. Immunotherapy in gastric cancer—A systematic review. Oncol Res. 2025;33(2):263–281. https://doi.org/10.32604/or.2024.052207

IEEE Style

M. SANTOS, D. MARTINS, and F. MENDES, “Immunotherapy in gastric cancer—A systematic review,” Oncol. Res., vol. 33, no. 2, pp. 263–281, 2025. https://doi.org/10.32604/or.2024.052207

Exosomal miR-224-3p promotes lymphangiogenesis and lymph node metastasis by targeting GSK3B in gastric cancer

外泌体miR-224-3p通过靶向GSK3B促进胃癌的淋巴管生成和淋巴结转移

ZHENGYANG ZHOU, LEI QIAO, TONGTONG WANG, WEN PAN, JINGJING DUAN, HAIYANG ZHANG, TING DENG, YI BA, YI HE

Graphic Abstract

胃癌患者常发生淋巴结转移（LNM），这不仅是肿瘤复发的关键因素，也是预后不良的重要原因。近年来研究发现，外泌体在肿瘤淋巴管生成过程中发挥着关键作用。本研究通过血清测序筛选出与胃癌淋巴结转移相关的外泌体miRNA——miR-224-3p。实验结果表明，胃癌细胞来源的外泌体miR-224-3p可进入人淋巴内皮细胞（HLECs），促进其管腔形成和迁移能力，从而增强肿瘤淋巴管生成。机制上，miR-224-3p通过靶向抑制GSK3B，阻断β-catenin的磷酸化，增强转录因子PROX1的表达。此外，hnRNPA1参与了miR-224-3p向外泌体中的选择性包装，而PKM2的高表达促进了exo-miR-224-3p的分泌。该研究揭示的“exo-miR-224-3p/GSK3B/β-catenin/PROX1”轴为胃癌淋巴转移的治疗提供了新的潜在靶点。

引用格式：

APA Style

ZHOU, Z., QIAO, L., WANG, T., PAN, W., DUAN, J. et al. (2025). Exosomal miR-224-3p promotes lymphangiogenesis and lymph node metastasis by targeting GSK3B in gastric cancer. Oncology Research, 33(2), 327–345. https://doi.org/10.32604/or.2024.050431

Vancouver Style

ZHOU Z, QIAO L, WANG T, PAN W, DUAN J, ZHANG H, et al. Exosomal miR-224-3p promotes lymphangiogenesis and lymph node metastasis by targeting GSK3B in gastric cancer. Oncol Res. 2025;33(2):327–345. https://doi.org/10.32604/or.2024.050431

IEEE Style

Z. ZHOU et al., “Exosomal miR-224-3p promotes lymphangiogenesis and lymph node metastasis by targeting GSK3B in gastric cancer,” Oncol. Res., vol. 33, no. 2, pp. 327–345, 2025. https://doi.org/10.32604/or.2024.050431

SBL-JP-0004: A promising dual inhibitor of JAK2 and PI3KCD against gastric cancer

SBL-JP-0004：一种有望用于治疗胃癌的JAK2与PI3KCD双重抑制剂

HASSAN M. OTIFI

JAK2与PI3KCD的结构，显示可成药靶点口袋。

胃癌作为全球性健康难题，其高度异质性的分子特征及对传统疗法的耐药性，严重影响了治疗效果。本研究聚焦于JAK-STAT通路与PI3K信号通路，这两者在胃癌进展中具有关键作用。通过计算模拟和分子动力学研究，研究者发现SBL-JP-0004可作为JAK2与PI3KCD的双重抑制剂。体外实验显示，SBL-JP-0004对JAK2与PI3KCD均具有较强的结合能力和抑制活性，并显著抑制KATOIII和SNU-5胃癌细胞的增殖，同时诱导明显的早期和晚期凋亡反应。这些结果表明，SBL-JP-0004有望成为治疗胃癌的潜力靶向药物，值得进一步开展临床前和临床研究。

引用格式：

APA Style

OTIFI, H.M. (2025). SBL-JP-0004: A promising dual inhibitor of JAK2 and PI3KCD against gastric cancer. Oncology Research, 33(1), 235–243. https://doi.org/10.32604/or.2024.055677

Vancouver Style

OTIFI HM. SBL-JP-0004: A promising dual inhibitor of JAK2 and PI3KCD against gastric cancer. Oncol Res. 2025;33(1):235–243. https://doi.org/10.32604/or.2024.055677

IEEE Style

H. M. OTIFI, “SBL-JP-0004: A promising dual inhibitor of JAK2 and PI3KCD against gastric cancer,” Oncol. Res., vol. 33, no. 1, pp. 235–243, 2025. https://doi.org/10.32604/or.2024.055677

Gastric cancer secreted miR-214-3p inhibits the anti-angiogenesis effect of apatinib by suppressing ferroptosis in vascular endothelial cells

胃癌分泌的 miR-214-3p 通过抑制血管内皮细胞的铁死亡作用，削弱阿帕替尼的抗血管生成效果

WEIXUE WANG, TONGTONG WANG, YAN ZHANG, TING DENG, HAIYANG ZHANG, YI BA

胃癌分泌的 miR-214-3p 通过抑制血管内皮细胞中的铁死亡，从而削弱了阿帕替尼的抗血管生成作用。胃癌细胞分泌的外泌体富含 miR-214-3p，可进入血管内皮细胞并释放内容物，使细胞内 miR-214-3p 水平升高。随后，miR-214-3p 通过 miR-214-3p/A20/ACSL4 轴调控内皮细胞的铁死亡过程。同时，阿帕替尼也可直接作用于内皮细胞中的 ACSL4。然而，由于 miR-214-3p 的调控作用，最终导致阿帕替尼治疗失效。

本研究揭示，胃癌细胞分泌的外泌体携带 miR-214-3p，可进入血管内皮细胞并抑制铁死亡，削弱抗血管生成药物阿帕替尼的治疗效果。机制上，miR-214-3p 靶向抑制铁死亡关键酶 ACSL4，从而抑制脂质过氧化。抑制 miR-214-3p 可增强内皮细胞对阿帕替尼的敏感性，提示联合靶向 miR-214-3p 有望提高晚期胃癌治疗效果。

引用格式：

APA Style

WANG, W., WANG, T., ZHANG, Y., DENG, T., ZHANG, H. et al. (2024). Gastric cancer secreted miR-214-3p inhibits the anti-angiogenesis effect of apatinib by suppressing ferroptosis in vascular endothelial cells. Oncology Research, 32(3), 489–502. https://doi.org/10.32604/or.2023.046676

Vancouver Style

WANG W, WANG T, ZHANG Y, DENG T, ZHANG H, BA Y. Gastric cancer secreted miR-214-3p inhibits the anti-angiogenesis effect of apatinib by suppressing ferroptosis in vascular endothelial cells. Oncol Res. 2024;32(3):489–502. https://doi.org/10.32604/or.2023.046676

IEEE Style

W. WANG, T. WANG, Y. ZHANG, T. DENG, H. ZHANG, and Y. BA, “Gastric cancer secreted miR-214-3p inhibits the anti-angiogenesis effect of apatinib by suppressing ferroptosis in vascular endothelial cells,” Oncol. Res., vol. 32, no. 3, pp. 489–502, 2024. https://doi.org/10.32604/or.2023.046676

NAD+ associated genes as potential biomarkers for predicting the prognosis of gastric cancer

与NAD⁺相关的基因可作为预测胃癌预后的潜在生物标志物

XIANGDONG SUN, HUIJUAN WEN, FAZHAN LI, IHTISHAM BUKHARI, FEIFEI REN, XIA XUE, PENGYUAN ZHENG, YANG MI

Graphic Abstract

NAD⁺（烟酰胺腺嘌呤二核苷酸）在细胞代谢、线粒体稳态、炎症及衰老中起关键作用，但其调控的基因在胃癌发展中的作用仍不清晰。本研究构建了一个基于NAD⁺代谢相关基因（NMRGs）表达的预后预测模型，筛选出13个相关lncRNA，发现高风险评分患者预后较差，且免疫检查点基因上调，免疫细胞浸润水平显著相关。此外，使用NAD⁺前体NMN处理胃癌细胞后，细胞增殖增强，SASP因子表达显著下降。结果表明，NAD⁺代谢相关lncRNA有望成为预测胃癌患者临床预后的新型生物标志物。

引用格式：

APA Style

SUN, X., WEN, H., LI, F., BUKHARI, I., REN, F. et al. (2024). NAD+ associated genes as potential biomarkers for predicting the prognosis of gastric cancer. Oncology Research, 32(2), 283–296. https://doi.org/10.32604/or.2023.044618

Vancouver Style

SUN X, WEN H, LI F, BUKHARI I, REN F, XUE X, et al. NAD+ associated genes as potential biomarkers for predicting the prognosis of gastric cancer. Oncol Res. 2024;32(2):283–296. https://doi.org/10.32604/or.2023.044618

IEEE Style

X. SUN et al., “NAD+ associated genes as potential biomarkers for predicting the prognosis of gastric cancer,” Oncol. Res., vol. 32, no. 2, pp. 283–296, 2024. https://doi.org/10.32604/or.2023.044618

GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling

GIPC1通过激活PDGFR/PI3K/AKT信号通路促进胃癌的肿瘤生长和迁移

TINGTING LI, WEI ZHONG, LIU YANG, ZHIYU ZHAO, LI WANG, CONG LIU, WANYUN LI, HAIYAN LV, SHENGYU WANG, JIANGHUA YAN, TING WU, GANG SONG, FANGHONG LUO

胃癌（GC）死亡率高，亟需新的治疗靶点。本研究发现GIPC1在胃癌及其肝转移和淋巴结转移组织中表达升高。敲低或阻断GIPC1可抑制PDGFR/PI3K/AKT信号通路，进而抑制胃癌细胞的增殖和迁移；相反，GIPC1过表达则显著激活该通路，促进肿瘤生长与迁移。相关细胞因子PDGF-BB及AKT抑制剂可减弱GIPC1表达差异带来的效应。小鼠模型中，GIPC1沉默减少肿瘤生长和转移，过表达则促进。综上，GIPC1作为胃癌的癌基因，通过PDGFR/PI3K/AKT通路调控细胞增殖与迁移，具有潜在治疗价值。

引用格式：

APA Style

LI, T., ZHONG, W., YANG, L., ZHAO, Z., WANG, L. et al. (2024). GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling. Oncology Research, 32(2), 361–371. https://doi.org/10.32604/or.2023.043807

Vancouver Style

LI T, ZHONG W, YANG L, ZHAO Z, WANG L, LIU C, et al. GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling. Oncol Res. 2024;32(2):361–371. https://doi.org/10.32604/or.2023.043807

IEEE Style

T. LI et al., “GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling,” Oncol. Res., vol. 32, no. 2, pp. 361–371, 2024. https://doi.org/10.32604/or.2023.043807

High-throughput computational screening and in vitro evaluation identifies 5-(4-oxo-4H-3,1-benzoxazin-2-yl)-2-[3-(4-oxo-4H-3,1-benzoxazin-2-yl) phenyl]-1H-isoindole-1,3(2H)-dione (C3), as a novel EGFR—HER2 dual inhibitor in gastric tumors

高通量计算筛选与体外评估鉴定出5-(4-氧代-4H-3,1-苯并恶唑啉-2-基)-2-[3-(4-氧代-4H-3,1-苯并恶唑啉-2-基)苯基]-1H-异茚-1,3(2H)-二酮（C3）作为一种新型胃肿瘤表皮生长因子受体（EGFR）与人表皮生长因子受体2（HER2）双重抑制剂

MESFER AL SHAHRANI, REEM GAHTANI, MOHAMMAD ABOHASSAN, MOHAMMAD ALSHAHRANI, YASSER ALRAEY, AYED DERA, MOHAMMAD RAJEH ASIRI, PRASANNA RAJAGOPALAN

Graphic Abstract

胃癌主要由表皮生长因子受体（EGFR）和人表皮生长因子受体2（HER2）激酶的激活和扩增引起，促进细胞增殖、粘附、血管生成和转移。由于肿瘤内部异质性和伴随的基因突变，传统疗法效果有限，因而推荐采用双重抑制策略以提高疗效并减少毒性。本研究通过高通量计算筛选ChemBridge小分子库，结合体外实验，发现了新型选择性EGFR/HER2双重抑制剂。分子动力学模拟和自由能计算确认化合物C3对EGFR和HER2具有良好亲和力。C3对EGFR和HER2激酶的IC50分别为37.24 nM和45.83 nM，对胃癌细胞系KATOIII和Snu-5的GI50分别为84.76 nM和48.26 nM。结果表明，C3具有潜在的双重抑制活性，是胃癌治疗的有前景的先导分子，但仍需进一步药代动力学及更高模型的验证。

引用格式：

APA Style

SHAHRANI, M.A., GAHTANI, R., ABOHASSAN, M., ALSHAHRANI, M., ALRAEY, Y. et al. (2024). High-throughput computational screening and in vitro evaluation identifies 5-(4-oxo-4H-3,1-benzoxazin-2-yl)-2-[3-(4-oxo-4H-3,1-benzoxazin-2-yl) phenyl]-1H-isoindole-1,3(2H)-dione (C3), as a novel EGFR—HER2 dual inhibitor in gastric tumors. Oncology Research, 32(2), 251–259. https://doi.org/10.32604/or.2023.043139

Vancouver Style

SHAHRANI MA, GAHTANI R, ABOHASSAN M, ALSHAHRANI M, ALRAEY Y, DERA A, et al. High-throughput computational screening and in vitro evaluation identifies 5-(4-oxo-4H-3,1-benzoxazin-2-yl)-2-[3-(4-oxo-4H-3,1-benzoxazin-2-yl) phenyl]-1H-isoindole-1,3(2H)-dione (C3), as a novel EGFR—HER2 dual inhibitor in gastric tumors. Oncol Res. 2024;32(2):251–259. https://doi.org/10.32604/or.2023.043139

IEEE Style

M. A. SHAHRANI et al., “High-throughput computational screening and in vitro evaluation identifies 5-(4-oxo-4H-3,1-benzoxazin-2-yl)-2-[3-(4-oxo-4H-3,1-benzoxazin-2-yl) phenyl]-1H-isoindole-1,3(2H)-dione (C3), as a novel EGFR—HER2 dual inhibitor in gastric tumors,” Oncol. Res., vol. 32, no. 2, pp. 251–259, 2024. https://doi.org/10.32604/or.2023.043139

The SMAD2/miR-4256/HDAC5/p16INK4a signaling axis contributes to gastric cancer progression

SMAD2/miR-4256/HDAC5/p16INK4a信号轴促进胃癌进展

MIN WANG, HAILIANG ZHAO, WEIWEI CHEN, CAIQUN BIE, JINYING YANG, WENRUI CAI, CHUTIAN WU, YANFANG CHEN, SHUFEN FENG, YING SHI, YUTING LI, HUIJUN TANG, LIXIAN ZHONG, LILIANGZI GUO, SISI CHEN, LINJING LONG, SHAOHUI TANG

Graphic Abstract

外泌体微小RNA（miRNA）的失调在癌症发展中起重要作用。本研究发现血清外泌体miR-4256在胃癌（GC）中显著上调，且促进肿瘤生长与进展。机制上，miR-4256通过靶向HDAC5基因启动子增强HDAC5表达，进而通过HDAC5对p16INK4a启动子进行表观遗传调控，抑制p16INK4a表达。此外，SMAD2/p300复合体正向调控miR-4256的表达。该SMAD2/miR-4256/HDAC5/p16INK4a信号轴促进胃癌进展，具有潜在的治疗和预后价值。

引用格式：

APA Style

WANG, M., ZHAO, H., CHEN, W., BIE, C., YANG, J. et al. (2023). The SMAD2/miR-4256/HDAC5/p16INK4a signaling axis contributes to gastric cancer progression. Oncology Research, 31(4), 515–541. https://doi.org/10.32604/or.2023.029101

Vancouver Style

WANG M, ZHAO H, CHEN W, BIE C, YANG J, CAI W, et al. The SMAD2/miR-4256/HDAC5/p16INK4a signaling axis contributes to gastric cancer progression. Oncol Res. 2023;31(4):515–541. https://doi.org/10.32604/or.2023.029101

IEEE Style

M. WANG et al., “The SMAD2/miR-4256/HDAC5/p16INK4a signaling axis contributes to gastric cancer progression,” Oncol. Res., vol. 31, no. 4, pp. 515–541, 2023. https://doi.org/10.32604/or.2023.029101

YWHAH activates the HMGA1/PI3K/AKT/mTOR signaling pathway by positively regulating Fra-1 to affect the proliferation of gastric cancer cells

YWHAH通过正向调控Fra-1激活HMGA1/PI3K/AKT/mTOR信号通路，进而影响胃癌细胞的增殖

JUNYU HE, FENG ZENG, XI JIN, LIN LIANG, MENGXIANG GAO, WENTAO LI, GUIYUAN LI, YANHONG ZHOU

YWHAH与Fra-1相互作用对胃癌细胞增殖影响的示意图。

Fos相关抗原1（Fra-1）是一种调控细胞生长、分化和凋亡的核转录因子，参与恶性肿瘤细胞的增殖、侵袭、凋亡及上皮-间质转化。Fra-1在胃癌（GC）中高表达，影响细胞周期分布和凋亡，参与胃癌发生发展，但其具体机制尚不明确。本研究通过免疫共沉淀结合液相色谱-串联质谱鉴定出YWHAH为胃癌细胞中与Fra-1相互作用的蛋白。实验表明YWHAH正向调控Fra-1的mRNA和蛋白表达，影响胃癌细胞增殖。全蛋白组分析显示Fra-1调控高迁移率族蛋白AT钩1（HMGA1）/磷脂酰肌醇-3-激酶（PI3K）/蛋白激酶B（AKT）/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路活性。Western印迹和流式细胞术证实YWHAH通过正向调控Fra-1激活HMGA1/PI3K/AKT/mTOR信号通路，促进胃癌细胞增殖。该研究为胃癌早期诊断、治疗及预后预测提供了潜在的新分子靶点。

引用格式：

APA Style

HE, J., ZENG, F., JIN, X., LIANG, L., GAO, M. et al. (2023). YWHAH activates the HMGA1/PI3K/AKT/mTOR signaling pathway by positively regulating Fra-1 to affect the proliferation of gastric cancer cells. Oncology Research, 31(4), 615–630. https://doi.org/10.32604/or.2023.029698

Vancouver Style

HE J, ZENG F, JIN X, LIANG L, GAO M, LI W, et al. YWHAH activates the HMGA1/PI3K/AKT/mTOR signaling pathway by positively regulating Fra-1 to affect the proliferation of gastric cancer cells. Oncol Res. 2023;31(4):615–630. https://doi.org/10.32604/or.2023.029698

IEEE Style

J. HE et al., “YWHAH activates the HMGA1/PI3K/AKT/mTOR signaling pathway by positively regulating Fra-1 to affect the proliferation of gastric cancer cells,” Oncol. Res., vol. 31, no. 4, pp. 615–630, 2023. https://doi.org/10.32604/or.2023.029698

Exploring the correlation and mechanism of natural killer cell cytotoxic sensitivity against gastric cancer

探索自然杀伤细胞对胃癌细胞毒性敏感性的相关性及其机制

WENZHUO YANG, HAODONG CHEN, ZHILAN ZHANG, ZHIYONG XIA, YUANYUAN JIN, ZHAOYONG YANG

脐带血来源NK细胞表型的流式细胞术分析。

(A) CD3⁻CD56⁺ NK细胞上NKG2A、TIGIT和PD-1的表达；

(B) CD3⁻CD56⁺ NK细胞上NKG2D、CD226和CD16的表达；

自然杀伤细胞（NK细胞）作为一种有前景的过继性细胞治疗（ACT）手段，在肿瘤免疫治疗中备受关注，但其在实体瘤患者中的疗效仍受限。为提升NK细胞在胃癌治疗中的作用，本研究系统探讨了三种胃癌细胞系（AGS、HGC-27 和 NCI-N87）对脐带血来源NK细胞（UCB-NK）介导的细胞毒作用的敏感性机制。实验结果显示，高表达CD56的HGC-27细胞对NK细胞最为敏感。抑制CD56表达会降低NK细胞的杀伤效率。同时，联合奥沙利铂处理可增强NK细胞的抗肿瘤效应，机制可能与奥沙利铂诱导胃癌细胞表面NKG2D配体（NKG2DL）上调有关。该研究揭示，CD56和NKG2DL的表达水平分别影响胃癌细胞对NK细胞的敏感性和杀伤效率，为提升NK细胞免疫疗法在胃癌中的临床应用提供了新的策略和理论依据。

引用格式：

APA Style

YANG, W., CHEN, H., ZHANG, Z., XIA, Z., JIN, Y. et al. (2025). Exploring the correlation and mechanism of natural killer cell cytotoxic sensitivity against gastric cancer. Oncology Research, 33(6), 1485–1494. https://doi.org/10.32604/or.2025.059426

Vancouver Style

YANG W, CHEN H, ZHANG Z, XIA Z, JIN Y, YANG Z. Exploring the correlation and mechanism of natural killer cell cytotoxic sensitivity against gastric cancer. Oncol Res. 2025;33(6):1485–1494. https://doi.org/10.32604/or.2025.059426

IEEE Style

W. YANG, H. CHEN, Z. ZHANG, Z. XIA, Y. JIN, and Z. YANG, “Exploring the correlation and mechanism of natural killer cell cytotoxic sensitivity against gastric cancer,” Oncol. Res., vol. 33, no. 6, pp. 1485–1494, 2025. https://doi.org/10.32604/or.2025.059426

Classical biomarkers and non-coding RNAs associated with diagnosis and treatment in gastric cancer

与胃癌诊断和治疗相关的经典生物标志物与非编码RNA

JINGDAN QUAN, ZIXIN WAN, WEI WU, XINYUAN CAO, JIAYUAN QIU, XIAOYE LIU, ZHIWEI ZHANG

Correa级联假说认为，正常胃黏膜细胞可逐步发生恶变，其演变过程包括：由幽门螺杆菌感染引发的正常胃黏膜损伤，发展为非萎缩性胃炎、慢性萎缩性胃炎、肠化（癌前病变）、异型增生，最终进展为肠型胃癌。而弥漫型胃癌的发生也可能与幽门螺杆菌感染有关，这通常是慢性活动性胃炎直接导致的结果。

胃癌在全球范围内高发，尤其在中国，早发型胃癌病例逐年上升。尽管已有手术和化疗等治疗手段，但晚期胃癌预后差，5年生存率仅为30%–35%。当前诊断多依赖胃镜和活检，侵入性强，患者不适感大。随着研究深入，免疫检查点抑制剂和非编码RNA被发现可作为新的诊断和治疗靶点。部分非编码RNA在胃癌患者血清或尿液中高表达，具有良好的无创诊断潜力，并在临床试验中展现出治疗效果。本文综述了胃癌诊疗相关的经典标志物与新兴非编码RNA，为实现更精准、高效的胃癌管理提供参考。

引用格式：

APA Style

QUAN, J., WAN, Z., WU, W., CAO, X., QIU, J. et al. (2025). Classical biomarkers and non-coding RNAs associated with diagnosis and treatment in gastric cancer. Oncology Research, 33(5), 1069–1089. https://doi.org/10.32604/or.2025.063005

Vancouver Style

QUAN J, WAN Z, WU W, CAO X, QIU J, LIU X, et al. Classical biomarkers and non-coding RNAs associated with diagnosis and treatment in gastric cancer. Oncol Res. 2025;33(5):1069–1089. https://doi.org/10.32604/or.2025.063005

IEEE Style

J. QUAN et al., “Classical biomarkers and non-coding RNAs associated with diagnosis and treatment in gastric cancer,” Oncol. Res., vol. 33, no. 5, pp. 1069–1089, 2025. https://doi.org/10.32604/or.2025.063005

A novel Wnt/β-catenin signaling gene signature for progression and metastasis of gastric cancer

一种用于预测胃癌进展与转移的新型Wnt/β-catenin信号通路基因特征签名

JIA CHEN, FEI JIANG, KAIYI NIU, HAODONG ZHAO, LI LI, HONGZHU YU

AEBP1工作流程图：上游的CPZ（羧肽酶Z）转录因子AEBP1（脂肪细胞增强子结合蛋白1）与下游Wnt信号通路转录因子TCF3（转录因子3）在细胞核内协同作用，共同增强与CPZ共表达基因及Wnt信号通路相关基因的表达，包括WNT2/FZD2（Wnt家族成员2/Frizzled类受体2）和上皮-间质转化（EMT）标志物VIM（波形蛋白）。该过程促进了胃癌细胞的侵袭、迁移和恶性转移。

Wnt/β-catenin信号通路在癌症的恶性进展、转移和耐药过程中常常出现失调，特别是在胃癌中，其异常活化与不良预后密切相关。本研究通过LASSO回归分析筛选出与Wnt通路相关的五个预后基因标志物，包括CPZ、CTHRC1、DKK1、EGF和GPC3，构建了可预测胃癌患者风险评分的基因特征模型。研究还发现，转录因子AEBP1与TCF3可在细胞核内协同作用，激活WNT2/FZD2与VIM等关键下游基因，促进胃癌细胞的迁移、侵袭和恶性转移。本文不仅提供了一个精准的预后预测模型，还揭示了AEBP1-TCF3轴在胃癌转移中的潜在作用，为靶向治疗提供了新的方向。

引用格式：

APA Style

CHEN, J., JIANG, F., NIU, K., ZHAO, H., LI, L. et al. (2025). A novel Wnt/β-catenin signaling gene signature for progression and metastasis of gastric cancer. Oncology Research, 33(5), 1199–1215. https://doi.org/10.32604/or.2024.054366

Vancouver Style

CHEN J, JIANG F, NIU K, ZHAO H, LI L, YU H. A novel Wnt/β-catenin signaling gene signature for progression and metastasis of gastric cancer. Oncol Res. 2025;33(5):1199–1215. https://doi.org/10.32604/or.2024.054366

IEEE Style

J. CHEN, F. JIANG, K. NIU, H. ZHAO, L. LI, and H. YU, “A novel Wnt/β-catenin signaling gene signature for progression and metastasis of gastric cancer,” Oncol. Res., vol. 33, no. 5, pp. 1199–1215, 2025. https://doi.org/10.32604/or.2024.054366

KHSRP promotes cancer stem cell maintenance, tumorigenesis, and suppresses anti-tumor immunity in gastric cancer

KHSRP在胃癌中促进癌症干细胞维持、肿瘤发生，并抑制抗肿瘤免疫

YARU DU, ZHIHUI PEI, SHUQIN HU, CHUANWEN LIAO, SHUHAO LIU

本研究聚焦于RNA结合蛋白KHSRP（KH结构域剪接调控蛋白）在胃癌中的作用。通过TCGA数据库和组织免疫组化分析发现，KHSRP在胃癌组织中高表达，并与肿瘤分期升高和患者预后不良密切相关。功能实验显示，KHSRP可促进胃癌细胞的增殖、干性维持及迁移能力。在小鼠模型中，敲低KHSRP不仅抑制了肿瘤生长，还增强了免疫细胞的浸润。该研究揭示了KHSRP在胃癌中的致瘤功能及其对抗肿瘤免疫的抑制作用，提示其可能成为胃癌的预后生物标志物和治疗新靶点。

引用格式：

APA Style

DU, Y., PEI, Z., HU, S., LIAO, C., LIU, S. (2025). KHSRP promotes cancer stem cell maintenance, tumorigenesis, and suppresses anti-tumor immunity in gastric cancer. Oncology Research, 33(2), 309–325. https://doi.org/10.32604/or.2024.058273

Vancouver Style

DU Y, PEI Z, HU S, LIAO C, LIU S. KHSRP promotes cancer stem cell maintenance, tumorigenesis, and suppresses anti-tumor immunity in gastric cancer. Oncol Res. 2025;33(2):309–325. https://doi.org/10.32604/or.2024.058273

IEEE Style

Y. DU, Z. PEI, S. HU, C. LIAO, and S. LIU, “KHSRP promotes cancer stem cell maintenance, tumorigenesis, and suppresses anti-tumor immunity in gastric cancer,” Oncol. Res., vol. 33, no. 2, pp. 309–325, 2025. https://doi.org/10.32604/or.2024.058273

lncRNA SNHG4 enhanced gastric cancer progression by modulating miR-409-3p/CREB1 axis

lncRNA SNHG4 通过调控 miR-409-3p/CREB1 轴促进胃癌进展

ZHOUYANG CHENG, YUCHEN HUA, YANG CAO, JUN QIN

胃癌作为全球高发且致死率高的恶性肿瘤，其分子机制的研究为诊断和治疗提供了新的方向。本研究发现长链非编码RNA SNHG4在胃癌组织及细胞中高表达，且与患者较差的生存率相关。功能实验显示，SNHG4促进胃癌细胞的增殖、迁移和侵袭，同时抑制细胞凋亡和细胞周期阻滞，促进肿瘤生长。机制研究表明，SNHG4通过吸附miR-409-3p，解除其对转录因子CREB1的抑制作用，进而促进胃癌进展。该发现有助于深化对胃癌发生发展的理解，为潜在的治疗策略提供新靶点。

引用格式：

APA Style

CHENG, Z., HUA, Y., CAO, Y., QIN, J. (2025). lncRNA SNHG4 enhanced gastric cancer progression by modulating miR-409-3p/CREB1 axis. Oncology Research, 33(1), 185–198. https://doi.org/10.32604/or.2024.042281

Vancouver Style

CHENG Z, HUA Y, CAO Y, QIN J. lncRNA SNHG4 enhanced gastric cancer progression by modulating miR-409-3p/CREB1 axis. Oncol Res. 2025;33(1):185–198. https://doi.org/10.32604/or.2024.042281

IEEE Style

Z. CHENG, Y. HUA, Y. CAO, and J. QIN, “lncRNA SNHG4 enhanced gastric cancer progression by modulating miR-409-3p/CREB1 axis,” Oncol. Res., vol. 33, no. 1, pp. 185–198, 2025. https://doi.org/10.32604/or.2024.042281

The effect of celastrol in combination with 5-fluorouracil on proliferation and apoptosis of gastric cancer cell lines

雷公藤内酯与5-氟尿嘧啶联合对胃癌细胞系增殖和凋亡的影响

MOHAMMAD-TAGHI MORADI, DHIYA ALTEMEMY, MAJID ASADI-SAMANI, PEGAH KHOSRAVIAN, MARZIYEH SOLTANI, LEILA HASHEMI, AZADEH SAMIEI-SEFAT

尽管5-氟尿嘧啶（5-FU）等化疗药物广泛应用于胃癌治疗，但药物耐药和副作用仍限制了其疗效。本研究探讨了雷公藤内酯（celastrol）与5-FU联合使用对胃癌细胞系（AGS和EPG85-257）增殖及凋亡的影响。结果显示，低浓度雷公藤内酯联合5-FU显著降低了两种细胞的IC50值，增强了抑制效果。联合治疗还显著提高了细胞凋亡率，并诱导细胞周期在合成期阻滞。研究表明，雷公藤内酯可增强5-FU的抗癌活性，但仍需更多研究以确认其抗肿瘤作用的具体机制。

引用格式：

APA Style

MORADI, M., ALTEMEMY, D., ASADI-SAMANI, M., KHOSRAVIAN, P., SOLTANI, M. et al. (2024). The effect of celastrol in combination with 5-fluorouracil on proliferation and apoptosis of gastric cancer cell lines. Oncology Research, 32(7), 1231–1237. https://doi.org/10.32604/or.2024.047187

Vancouver Style

MORADI M, ALTEMEMY D, ASADI-SAMANI M, KHOSRAVIAN P, SOLTANI M, HASHEMI L, et al. The effect of celastrol in combination with 5-fluorouracil on proliferation and apoptosis of gastric cancer cell lines. Oncol Res. 2024;32(7):1231–1237. https://doi.org/10.32604/or.2024.047187

IEEE Style

M. MORADI et al., “The effect of celastrol in combination with 5-fluorouracil on proliferation and apoptosis of gastric cancer cell lines,” Oncol. Res., vol. 32, no. 7, pp. 1231–1237, 2024. https://doi.org/10.32604/or.2024.047187

The Epstein-Barr virus-miRNA-BART6-5p regulates TGF-β/SMAD4 pathway to induce glycolysis and enhance proliferation and metastasis of gastric cancer cells

Epstein-Barr病毒miRNA-BART6-5p调控TGF-β/SMAD4通路，促进糖酵解并增强胃癌细胞的增殖和转移

XUHUI ZHAO, XIAOMIN HUANG, CHUNYAN DANG, XIA WANG, YUJIAO QI, HONGLING LI

EBV相关miRNA-BARTs在上皮肿瘤，特别是EB病毒相关的胃癌和鼻咽癌中扮演重要角色，但其在胃癌发生发展中的具体机制尚不清楚。本研究发现EBV-miRNA-BART6-5p在EB病毒相关胃癌组织和细胞中显著上调，而其靶基因SMAD4表达下调。EBV-miRNA-BART6-5p的上调促进胃癌细胞的增殖、迁移及糖酵解过程。抑制TGF-β/SMAD4信号通路能降低胃癌细胞的增殖和迁移能力，同时减弱糖酵解活性。研究表明，EBV-miRNA-BART6-5p通过调控TGF-β/SMAD4通路，靶向SMAD4，增强胃癌细胞的糖代谢，促进其恶性进展。这为胃癌代谢机制的深入理解提供了新视角。

引用格式：

APA Style

ZHAO, X., HUANG, X., DANG, C., WANG, X., QI, Y. et al. (2024). The Epstein-Barr virus-miRNA-BART6-5p regulates TGF-β/SMAD4 pathway to induce glycolysis and enhance proliferation and metastasis of gastric cancer cells. Oncology Research, 32(5), 999–1009. https://doi.org/10.32604/or.2024.046679

Vancouver Style

ZHAO X, HUANG X, DANG C, WANG X, QI Y, LI H. The Epstein-Barr virus-miRNA-BART6-5p regulates TGF-β/SMAD4 pathway to induce glycolysis and enhance proliferation and metastasis of gastric cancer cells. Oncol Res. 2024;32(5):999–1009. https://doi.org/10.32604/or.2024.046679

IEEE Style

X. ZHAO, X. HUANG, C. DANG, X. WANG, Y. QI, and H. LI, “The Epstein-Barr virus-miRNA-BART6-5p regulates TGF-β/SMAD4 pathway to induce glycolysis and enhance proliferation and metastasis of gastric cancer cells,” Oncol. Res., vol. 32, no. 5, pp. 999–1009, 2024. https://doi.org/10.32604/or.2024.046679

Apolipoprotein C1 promotes tumor progression in gastric cancer

载脂蛋白C1促进胃癌肿瘤进展

QIOU GU, TIAN ZHAN, XIAO GUAN, CHUILIN LAI, NA LU, GUOGUANG WANG, LEI XU, XIANG GAO, JIANPING ZHANG

胃癌（GC）是预后极差且严重威胁人类健康的恶性肿瘤，尤其在东亚地区高发。载脂蛋白C1（apoc1）作为载脂蛋白家族成员，虽与多种肿瘤相关，但其在胃癌中的作用尚不清楚。本研究基于TCGA数据库发现apoc1在胃癌中高表达且与预后不良显著相关，且其表达水平与肿瘤分级、分期和浸润深度呈正相关。功能实验表明apoc1促进胃癌细胞的侵袭和迁移。GO、KEGG和GSEA分析提示apoc1可能参与WNT信号通路及免疫调控。肿瘤微环境分析显示apoc1与免疫细胞浸润密切相关。此外，apoc1表达还与药物敏感性及免疫检查点抑制剂（PD-1和CTLA-4）治疗相关。综上，apoc1参与胃癌进展，有望成为诊断及免疫治疗的潜在靶点。

引用格式：

APA Style

GU, Q., ZHAN, T., GUAN, X., LAI, C., LU, N. et al. (2023). Apolipoprotein C1 promotes tumor progression in gastric cancer. Oncology Research, 31(3), 287–297. https://doi.org/10.32604/or.2023.028124

Vancouver Style

GU Q, ZHAN T, GUAN X, LAI C, LU N, WANG G, et al. Apolipoprotein C1 promotes tumor progression in gastric cancer. Oncol Res. 2023;31(3):287–297. https://doi.org/10.32604/or.2023.028124

IEEE Style

Q. GU et al., “Apolipoprotein C1 promotes tumor progression in gastric cancer,” Oncol. Res., vol. 31, no. 3, pp. 287–297, 2023. https://doi.org/10.32604/or.2023.028124

OR 期刊简介

主编

Edward Chu, Albert Einstein College of Medicine, USA

Enrico Mini, University of Florence, ITALY

Hailin Tang, Sun Yat-Sen University Cancer Center, CHINA

Oncology Research是由美国Tech Science Press出版社发行的一本关注癌症治疗的国际英文期刊。重点关注的领域包括开发新型小分子和靶向治疗的临床前和转化研究;药物敏感机制;细胞耐药机制;反应和/或耐药的生物标志物;与癌症治疗相关的新型实验模型系统和技术;药物遗传学和药物基因组学;个性化医学;免疫治疗和临床免疫学;基因治疗等。目前被SCI (Web of Science), Scopus, PubMed等一些世界主要引文数据库收录。

官方邮箱：oncologyresearch@techscience.com

期刊链接：https://www.techscience.com/journal/or

发布于：中国香港

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