MiR-126、血管内皮生长因子的表达与微血管密度在上皮性卵巢癌组织中的变化

目的 探讨miR-126、血管内皮生长因子(VEGF)的表达与微血管密度(MVD)在上皮性卵巢癌组织中的变化及意义.方法 采用qRT-PCR检测21例正常卵巢组织、23例良性卵巢肿瘤组织及45例上皮性卵巢癌组织中miR-126表达水平,采用免疫组化法检测VEGF蛋白表达及MVD.结果 MiR-126在上皮性卵巢癌组织中的表达明显低于正常卵巢组织、良性卵巢肿瘤组织(P<0.05);VEGF阳性率和MVD在上皮性卵巢癌组织中明显高于正常卵巢组织、良性卵巢肿瘤组织(P<0.05).上皮性卵巢癌组织中miR-126、VEGF及MVD与FIGO分期、淋巴结转移有关(P<0.05).结论 MiR-126、VEGF可能与上皮性卵巢癌的发生、发展、肿瘤异常血管营养及侵袭转移有关.     

上皮性卵巢癌中内皮抑素与血管内皮生长因子的表达及意义

目的:探讨内皮抑素(Endostatin)及血管内皮生长因子(VEGF)在上皮性卵巢组织中的表达及意义。方法:采用免疫组化SP法检测48例上皮性卵巢癌组织、18例良性上皮性卵巢肿瘤及18例正常卵巢组织中Endostatin及VEGF的表达。结果:1)卵巢癌组织Endostatin和VEGF表达明显高于良性卵巢瘤和正常卵巢组织(P<0.05)。2)48例上皮性卵巢癌组织中Endostatin及VEGF的阳性表达率分别为62.5%(30/48)和66.67%(36/48),Endostatin与VEGF的表达呈正相关。3)在晚期卵巢癌组织中Endostatin的高表达率及VEGF阳性率明显高于早期卵巢癌组织,差异具有显著性(P<0.05)。4)卵巢癌组织中Endostatin高表达和VEGF阳性患者的平均总生存期短于Endostatin低表达和VEGF阴性患者,但二者累计生存率均无显著性差异(P>0.05)。结论:Endostatin与VEGF的表达水平随着卵巢癌临床分期的进展而升高,反映了卵巢癌疾病发展过程中血管生成抑制因子和促进因子之间的平衡调节。     

CXCR4和MMP-2在卵巢上皮性肿瘤中的表达及意义

目的研究CXCR4和MMP-2在卵巢上皮性肿瘤中的表达情况及临床意义。方法应用免疫组织化学方法检测正常卵巢组织、良性上皮性卵巢瘤、卵巢癌、卵巢癌盆腔腹膜转移灶中CXCR4和MMP-2的表达,分析其与卵巢癌生物学特征之间的关系。结果CXCR4在卵巢癌及转移灶中的阳性率分别为60%、77.8%,明显高于正常卵巢组织（0）及卵巢良性肿瘤（0）;MMP-2在卵巢癌及转移灶中阳性率分别为85%、100%,明显高于正常卵巢组织（20%）及卵巢良性肿瘤（30%）（P均＜0.05）。两者的表达呈正相关。结论CXCR4和MMP-2在卵巢癌中表达明显上调,可能在卵巢癌发生发展过程中起重要作用。     

MTDH和VEGF在上皮性卵巢癌中的表达及临床意义

目的 探讨异黏蛋白（MTDH）及血管内皮生长因子（VEGF）在上皮性卵巢癌中的表达及其与上皮性卵巢癌临床病理特征的关系。方法 采用逆转录 聚合酶链反应（RT-PCR）及免疫组化SP法检测42例上皮性卵巢癌组（恶性组）、20例卵巢良性上皮性肿瘤组织（良性组）及15例正常卵巢上皮组织（正常组）中MTDH和VEGF mRNA及蛋白的表达,分析两者表达与上皮性卵巢癌临床病理特征的关系。结果 MTDH和VEGF mRNA在恶性组中的相对表达量分别为0.672±0.115和0.714±0.129,显著高于良性组（0.324±0.041、0.251±0.039）和正常组（0.317±0.035、0.243±0.031）,差异均有统计学意义（P＜0.01）。MTDH及VEGF蛋白在恶性组中的阳性表达率分别为69.0％、80.9％,显著高于良性组（20.0％、35.0％）和正常组（13.3％、20.0％）,差异均有统计学意义（P＜0.01）。MTDH和VEGF mRNA及蛋白的表达与上皮性卵巢癌的临床分期、淋巴结转移有关（P＜0.05）,而与病理类型及分化程度无关（P＞0.05）。在上皮性卵巢癌中MTDH与VEGF蛋白的表达呈正相关（r=0.420,P＜0.01）。 结论 MTDH和VEGF表达与上皮性卵巢癌的发生、发展有关。     

肌成束蛋白-1在上皮性卵巢癌组织中的表达及临床意义

摘 要：［目的］ 研究肌成束蛋白-1（FSCN1）在上皮性卵巢癌组织中的表达及与预后相关性。［方法］ 选取2010年1月至2014年12月我院收治的120例卵巢肿瘤患者作为研究对象,包括80例上皮性卵巢癌,40例卵巢良性上皮肿瘤。采用免疫组化检测FSCN1在癌组织、癌旁组织和良性组织中的表达水平。免疫组化检测上皮间质转化（epithelial mesenchymal transformation,EMT）关键蛋白波形蛋白（vimentin）和E钙黏蛋白（E-cadherin）在卵巢癌组织中的表达水平。［结果］ FSCN1在卵巢癌组织中的高表达率（67.5%,54/80）明显高于癌旁组织（28.8%,21/73）和良性卵巢组织（12.5%,5/40） (χ2=41.02,P<0.001)。FSCN1表达水平与临床病理分期、淋巴结转移具有相关性（P=0.023;P=0.026）,FSCN1表达水平与Vimentin表达水平呈正相关（P=0.007）,而与E-cadherin表达水平呈负相关（P=0.006）。FSCN1高表达水平患者总生存率（27.5%）明显低于FSCN1低表达水平的患者（52.3%）（P=0.007）,FSCN1高表达是上皮性卵巢癌患者不良预后的独立风险因素（P=0.011）。［结论］ FSCN1在上皮性卵巢癌中高表达,且与卵巢癌的恶性程度密切和EMT相关,对于预测卵巢癌的预后具有一定的价值。     

上皮性卵巢肿瘤RASSF1A基因甲基化与蛋白表达的关系及意义

目的：检测上皮性卵巢肿瘤中RASSF1A基因启动子CpG岛的甲基化状态,并探讨基因异常甲基化与蛋白表达的关系及其意义。方法：运用甲基化特异性PCR（MSP）方法对62例上皮性卵巢癌、21例交界性囊腺瘤及30例良性囊腺瘤的RASSF1A基因启动子甲基化状态进行检测,免疫组化S-P法检测上述标本中RASSF1A蛋白表达,并结合肿瘤生物学行为进行分析。结果：上皮性卵巢癌组织、卵巢交界性囊腺瘤组织中RASSF1A基因启动子区甲基化率（58.06%、42.85%）显著高于卵巢良性囊腺瘤组织（13.33%）,差异有统计学意义（P〈0.05）。RASSF1A基因启动子区甲基化与上皮性卵巢癌的细胞分化程度和临床分期密切相关（P〈0.05）而与组织类型和患者年龄及绝经与否无相关性（P〉0.05）;RASSF1A基因甲基化与其蛋白表达下降一致。结论：卵巢癌组织中存在RASSF1A基因启动子CpG岛的异常甲基化,可能和该蛋白表达缺失的主要原因,是导致该基因失活的重要机制之一。     

卵巢浆液性囊腺癌中PD-L1的表达和血清CA125对评价恶性程度的意义

目的:研究PD-L1在卵巢浆液性囊腺癌中的表达,结合患者术前CA125值,探讨二者对评价肿瘤生物学恶性程度的意义。方法:应用免疫组织化学法检测36例卵巢浆液性囊腺癌和20例正常卵巢组织蜡块中PD-L1的表达情况,收集36例卵巢癌患者术前血清CA125值,分析卵巢癌组织PD-L1表达与卵巢癌临床病理特征的关系及术前血清CA125的相关性。结果:卵巢浆液性囊腺癌组织中PD-L1的阳性表达率为88.9%（32/36）,显著高于其在正常卵巢组织中的表达40.0%（8/20）,差异有统计学意义（P＜0.01）。分化程度G2-3级组中PD-L1的阳性率显著高于G1级组,PD-L1与 FIGO分期无明显相关性,与患者术前CA125值呈正相关（r=0.739,P＜0.01）。结论:PD-L1的表达与术前血清CA125的增高程度结合分析对判断卵巢浆液性囊腺癌的生物学恶性程度有重要意义。     

H3K9ac、H3K4me2在卵巢浆液性上皮性肿瘤中的表达及意义

目的:探讨组蛋白H3第9位赖氨酸残基乙酰化（H3K9ac）及组蛋白H3第4位赖氨酸残基二甲基化（H3K4me2）在卵巢浆液性囊腺瘤、卵巢交界性浆液性囊腺瘤和卵巢浆液性囊腺癌组织中蛋白表达与浆液性上皮性卵巢癌发生、发展的关系及两者之间有无相关性。方法:应用免疫组织化学链霉菌抗生物素蛋白-过氧化酶连接法（SP法）检测H3K9ac、H3K4me2在30例卵巢浆液性囊腺瘤组织、30例卵巢交界性浆液性囊腺瘤组织及40例卵巢浆液性囊腺癌组织中的表达,观察表达差异并进行统计学处理。结果:H3K9ac在卵巢浆液性囊腺瘤组织中阳性表达率为93.33%,在卵巢交界性浆液性囊腺瘤组织中阳性表达率为66.67%,在卵巢浆液性囊腺癌中阳性表达率为42.50%,良性、交界性、恶性组织间两两比较差异有统计学意义（P＜0.05）。在不同手术病理分期、不同组织学分级的卵巢浆液性囊腺癌组织中H3K9ac的阳性表达率有统计学差异（P＜0.05）。H3K4me2在卵巢浆液性囊腺瘤组织中阳性表达率为90%,在交界性浆液性囊腺瘤组织中阳性表达率为73.33%,在卵巢浆液性囊腺癌中阳性表达率为52.50%,良性与交界性、交界性与恶性组织间比较差异无统计学意义（P＞0.05）,良性与恶性组织间比较差异有统计学意义（P＜0.05）。在不同手术病理分期、不同组织学分级的卵巢浆液性囊腺癌组织中H3K4me2的阳性表达率无统计学差异（P＞0.05）。H3K9ac、H3K4me2在卵巢浆液性囊腺癌组织中的表达呈正相关（r=0.732,P＜0.001）。结论:H3K9ac、H3K4me2的低表达与浆液性上皮性卵巢癌的发生、发展有关,有可能成为浆液性上皮性卵巢癌诊断和治疗的新靶点。     

KLK10和VEGF在上皮性卵巢癌中的表达及意义

目的：探讨KLK10蛋白和VEGF 在上皮性卵巢癌中的表达及临床意义。方法：应用免疫组化法检测15例上皮性卵巢良性、20例交界性和56例恶性肿瘤中KLK10蛋白和VEGF的表达,分析KLK10蛋白和VEGF表达与上皮性卵巢癌临床病理及生存状态的关系。结果：(1)在卵巢癌组织中,KLK10和VEGF的表达率分别为85.71％(48/56)和82.14%(46/56);(2) KLK10和VEGF的表达与卵巢癌的临床分期、淋巴结转移、组织分化及5年生存率显著相关(P<0.05)。结论：(1) KLK10蛋白和VEGF在上皮性卵巢癌中异常高表达;其高表达与临床分期、病理分级、淋巴结转移和5年生存率显著相关。KLK10蛋白和VEGF在上皮性卵巢癌中表达呈正相关,可作为上皮性卵巢癌的预后标志物。     

血管内皮生长因子mRNA在上皮性卵巢癌中的表达及意义

目的 探讨血管内皮生长因子（vascular endothelial growth factor, VEGF） 核酸在上皮性卵巢癌组织中的表达及其与临床、病理特性之间的联系。方法上皮性卵巢癌31例，卵巢上皮性良性肿瘤17例及正常卵巢组织5例,采用原位杂交技术显示各类卵巢组织中VEGF mRNA的表达水平。结果上皮性卵巢癌组织的VEGF mRNA阳性表达率为48.39%（15/31）,显著高于良性肿瘤（P〈0.05）。上皮性卵巢癌中VEGF mRNA阳性表达率与淋巴结转移与否及腹水量密切相关（P〈0.05）。上皮性卵巢癌不同组织类型、病理分级及临床分期等指标均与VEGF mRNA阳性表达率无明显相关性（P〉0.05）。上皮性卵巢癌的预后与其组织中 VEGF mRNA阳性表达率亦无相关性（P〉0.05）。结论 VEGF mRNA在上皮性卵巢癌中的表达水平显著升高,且与淋巴结转移与否及腹水量密切相关，可作为卵巢癌侵袭性评估的指标之一。     

lncRNA ANCR对直肠癌细胞增殖和凋亡能力的影响及机制

目的 探讨长链非编码RNA（lncRNA）抗分化非编码RNA（ANCR）对结直肠癌（CRC）细胞生物学行为的影响及其作用机制。方法 收集50例CRC患者的癌组织和癌旁组织，通过RT-qPCR检测组织中ANCR和叉头框蛋白O1（FOXO1）的表达水平并进行Pearson相关性分析。利用RNA 拉下和RNA免疫沉淀实验（RIP）确认ANCR是否可与FOXO1相互作用。将经过慢病毒包装的ANCR和FOXO1慢病毒质粒转染至人CRC细胞系SW480细胞中，细胞分为6组：对照组（未转染），NC组（转染慢病毒质粒空载），ANCR组（转染 pHRi-ANCR），sh-ANCR组（转染pHRi-sh-ANCR），FOXO1组（pHRi-FOXO1），sh-ANCR + sh-FOXO1组（同时转染pHRi-sh-ANCR和pHRi-sh-FOXO1）。RT-qPCR检测过表达和抑制ANCR后FOXO1的表达水平，5-乙炔基-2′脱氧尿嘧啶核苷（EdU）标记技术和流式细胞术分别检测各组细胞增殖、细胞周期和细胞凋亡情况。Western blot检测B淋巴细胞瘤-2（BCL-2）、BCL2相关蛋白X（BAX）、细胞周期蛋白D1（cyclin D1）及人P27蛋白（P27）的表达情况。结果 与癌旁组织相比，CRC组织中ANCR表达明显增加，FOXO1表达明显减少（P<0.01），二者表达水平负相关（P<0.01）。ANCR能够结合并抑制FOXO1表达。与NC组相比，sh-ANCR组和FOXO1组细胞增殖数减少，细胞阻滞于G0/G1期，细胞凋亡数增多，BAX和P27增多，BCL-2和cyclin D1减少（P<0.05）。与sh-ANCR组相比，sh-ANCR + sh-FOXO1组上述指标得到逆转（P<0.05）。结论 lncRNA ANCR在CRC中表达升高并通过调控FOXO1的表达调控CRC细胞的细胞增殖和凋亡。     

Hypoxia-inducible factor-1 and transforming growth factor-β in tumor

Hypoxia-inducible factor-1 (HIF-1) is one of the most important hypoxia signal transmission factor, and it has been observed in many human tumors. HIF-1 could play a role of promoting tumor by regulating the expression level of transforming growth factor-β in vivo and in vitro, and then affecting the development and prognosis of tumor.     

Triple therapy with osimertinib,bevacizumab and cetuximab in EGFR-mutant lung cancer with HIF-1α/TGF-α expression

Osimertinib, a third generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, is the standard treatment for patients with lung cancer harboring EGFR T790M; however, acquired resistance is inevitable due to genetic and epigenetic changes in cancer cells. In addition, a recent randomized clinical trial revealed that the combination of osimertinib and bevacizumab failed to exhibit superior progression-free survival compared with osimertinib alone. The present study aimed to investigate the effect of triple therapy with osimertinib, bevacizumab and cetuximab in xenograft tumors with different initial tumor volumes (conventional model, 200 mm³ and large model, 500 mm³). The results demonstrated that osimertinib significantly inhibited tumor growth in both the conventional and large models; however, maximum tumor regression was attenuated in the large model in which hypoxia-inducible factor-1α (HIF-1α) and transforming growth factor-α (TGF-α) expression levels increased. Although the combination of osimertinib and bevacizumab exerted a greater inhibitory effect on tumor growth compared with osimertinib in the conventional model, the effect of this combination therapy was attenuated in the large model. TGF-α attenuated sensitivity to osimertinib in vitro; however, this negative effect was counteracted by the combination of osimertinib and cetuximab, but not osimertinib and bevacizumab. In the large xenograft tumor model, the triple therapy induced the greatest inhibitory effect on tumor growth compared with osimertinib alone and its combination with bevacizumab. Clinical trials of the triple therapy are required for patients with lung cancer with EGFR mutations and HIF-1α/TGF-α.     

恶性机械性肠梗阻临床诊疗

恶性机械性肠梗阻是晚期肿瘤常见并发症之一，通常以内科综合治疗为主。了解其病理生理机制（包括“不协调蠕动-组织水肿-不协调蠕动”及“分泌-扩张-分泌”恶性循环），明确梗阻的分类、亚型和完善肿瘤内科的系统评估（包括一般情况、脏器功能、肿瘤学评估、营养代谢及肠屏障功能）是其有效治疗的前提。治疗原则和目的是尽量减少，甚至解除机体肿瘤负荷，改善或根治肠梗阻所致不良症状、体征及肠功能异常，纠正水、电解质紊乱及营养代谢紊乱状态，最终改善患者生活质量及总生存。具体措施包括基础治疗、营养治疗和代谢调节、抗炎、减轻肠壁水肿、抑制消化道腺体分泌、修复肠道屏障及防治感染、抗肿瘤病因治疗及运动疗法、心理治疗。其中抗肿瘤病因治疗是临床中的难点，因恶性肠梗阻多伴随营养不良、一般情况差，难以耐受常规抗肿瘤治疗，抗肿瘤治疗上需兼顾肿瘤因素、营养状况及患者一般情况等，有效的抗肿瘤治疗是肠梗阻再通的基本保障。     

恶性肠梗阻患者的代谢紊乱

恶性肠梗阻是由恶性肿瘤引起的小肠或大肠梗阻,常见于卵巢癌及胃肠道肿瘤患者。恶性肠梗阻是由于肿瘤压迫、肿瘤细胞浸润自主神经、副肿瘤综合征或药物因素导致的急性或慢性肠道梗阻,是晚期肿瘤患者常见的致死性并发症之一。本文综合国内外进展探讨恶性肠梗阻患者的代谢紊乱情况及其机制,得出以下提示:恶性肠梗阻不仅引起葡萄糖、蛋白质、脂肪酸等宏量营养素的代谢紊乱,还会引起微量营养素代谢异常等。造成代谢紊乱的机制主要有肠道功能紊乱,肠道局部甚至全身发生炎性反应,肠道菌群紊乱及缺乏有效的营养治疗等因素。恶性肠梗阻患者发生代谢紊乱可能加剧肠梗阻的发展,更与患者的预后显著相关。临床决策中医生应重视患者的代谢情况,认识到代谢紊乱对恶性肠梗阻患者预后的影响,积极纠正代谢紊乱,提高患者的预后及生活质量。     

C1GALT1 in health and disease

O-linked glycosylation (O-glycosylation) and N-linked glycosylation (N-glycosylation) are the two most important forms of protein glycosylation, which is an important post-translational modification. The regulation of protein function involves numerous mechanisms, among which protein glycosylation is one of the most important. Core 1 synthase glycoprotein-N-acetylgalactosamine 3-β-galactosyltransferase 1 (C1GALT1) serves an important role in the regulation of O-glycosylation and is an essential enzyme for synthesizing the core 1 structure of mucin-type O-glycans. Furthermore, C1GALT1 serves a vital role in a number of biological functions, such as angiogenesis, platelet production and kidney development. Impaired C1GALT1 expression activity has been associated with different types of human diseases, including inflammatory or immune-mediated diseases, and cancer. O-glycosylation exists in normal tissues, as well as in tumor tissues. Previous studies have revealed that changes in the level of glycosyltransferase in different types of cancer may be used as potential therapeutic targets. Currently, numerous studies have reported the dual role of C1GALT1 in tumors (carcinogenesis and cancer suppression). The present review reports the role of C1GALT1 in normal development and human diseases. Since the mechanism and regulation of C1GALT1 and O-glycosylation remain elusive, further studies are required to elucidate their effects on development and disease.     

ERG deregulation induces IGF-1R expression in prostate cancer cells and affects sensitivity to anti-IGF-1R agents

Identifying patients who may benefit from targeted therapy is an urgent clinical issue in prostate cancer (PCa). We investigated the molecular relationship between TMPRSS2-ERG (T2E) fusion gene and insulin-like growth factor receptor (IGF-1R) to optimize the use of IGF-1R inhibitors.IGF-1R was analyzed in cell lines and in radical prostatectomy specimens in relation to T2E status. ERG binding to IGF-1R promoter was evaluated by chromatin immunoprecipitation (ChIP). Sensitivity to anti-IGF-1R agents was evaluated alone or in combination with anti-androgen abiraterone acetate in vitro at basal levels or upon ERG modulation.IGF-1R analysis performed in PCa cells or clinical samples showed that T2E expression correlated with higher IGF-1R expression at mRNA and protein levels. Genetic modulation of ERG directly affected IGF-1R protein levels in vitro. ChIP analysis showed that ERG binds IGF-1R promoter and that promoter occupancy is higher in T2E-positive cells. IGF-1R inhibition was more effective in cell lines expressing the fusion gene and combination of IGF-1R inhibitors with abiraterone acetate produced synergistic effects in T2E-expressing cells.Here, we provide the rationale for use of T2E fusion gene to select PCa patients for anti-IGF-1R treatments. The combination of anti-IGF-1R-HAbs with an anti-androgen therapy is strongly advocated for patients expressing T2E.     

小鼠前胃癌组织形成中VEGF和cyclin D1及p27^kip1的表达

目的：研究VEGF、cyclin D1和p27^kip1在小鼠前胃癌组织形成过程中的表达及意义，初步探讨维甲酸对小鼠前胃癌的干预机制。方法：建立ICR小鼠前胃癌模型，SABC法测定VEGF、cyclin D1和p27^kip1表达。结果：cyclin D1在小鼠前胃癌组织中的表达（64．7％）明显高于癌前期病变（29．4％）。X^2=4．3447，P=0．0371；VEGF表达在癌前期病变（47．1％）高于增生期病变（33．3％），X^2=4．836，P=0．0381；cyclin D1、p27^kip1和VEGF阳性表达与小鼠胃癌组织学分级无相关性。维甲酸抑制组癌及癌前期病变发生率（23．5％）低于单纯诱导组（76．9％），X^2=14．3549．P=0．0002。结论：VEGF、cyclin D1和p27^kip1是小鼠前胃癌组织形成过程中重要的分子事件；维甲酸对亚硝胺类致癌物诱发的小鼠前胃鳞状上皮癌及癌前期病变具有抑制作用，但与对VEGF、cyclin D1和p27^kip1表达的调控无明显相关。     

Down regulation of c-Myc and induction of an angiogenesis inhibitor, thrombospondin-1, by 5-FU in human colon cancer KM12C cells

5-FU is commonly used for treatment of various solid tumors including colon carcinoma. We have previously demonstrated that Egr-1 induced by 5-FU enhanced TSP-1 expression in human colon cancer KM12C cells. In this study, a Genechip analysis of KM12C cells treated with 5-FU revealed down-regulation of 924 genes and up-regulation of 460 genes. The decreased expression of c-Myc mRNA and phosphorylated c-Myc were detected and confirmed by RT-PCR and immunoblotting. Since 5-FU induced the expression of TSP-1, we examined the effect of c-Myc on the TSP-1 promoter. Deletion of the TSP-1 promoter region in which binding sites for c-Myc reside had no effect on the TSP-1 promoter activity induced by 5-FU. Meanwhile, 5-FU dose-dependently decreased the expression of miR-17-92 cluster. These findings suggest that 5-FU decreased the expression of c-Myc and consequently miR-17-92 cluster and increased the expression of TSP-1 mRNA.     

LAMC1 upregulation via TGFβ induces inflammatory cancer‐associated fibroblasts in esophageal squamous cell carcinoma via NF‐κB–CXCL1–STAT3

Cancer‐associated fibroblasts (CAF) are a heterogeneous cell population within the tumor microenvironment,and play an important role in tumor development. By regulating the heterogeneity of CAF, transforming growth factor β (TGFβ) influences tumor development. Here, we explored oncogenes regulated by TGFβ1 that are also involved in signaling pathways and interactions within the tumor microenvironment. We analyzed sequencing data of The Cancer Genome Atlas (TCGA) and our own previously established RNA microarray data ({"type":"entrez-geo","attrs":{"text":"GSE53625","term_id":"53625"}}GSE53625), as well as esophageal squamous cell carcinoma (ESCC) cell lines with or without TGFβ1 stimulation. We then focused on laminin subunit gamma 1 (LAMC1), which was overexpressed in ESCC cells, affecting patient prognosis, which could be upregulated by TGFβ1 through the synergistic activation of SMAD family member 4 (SMAD4) and SP1. LAMC1 directly promoted the proliferation and migration of tumor cells, mainly via Akt–NFκB–MMP9/14 signaling. Additionally, LAMC1 promoted CXCL1 secretion, which stimulated the formation of inflammatory CAF (iCAF) through CXCR2–pSTAT3. Inflammatory CAF promoted tumor progression. In summary, we identified the dual mechanism by which the upregulation of LAMC1 by TGFβ in tumor cells not only promotes ESCC proliferation and migration, but also indirectly induces carcinogenesis by stimulating CXCL1 secretion to promote the formation of iCAF. This finding suggests that LAMC1 could be a potential therapeutic target and prognostic marker for ESCC.