{"title":"子宫内膜癌的预后标志物Mark3。","authors":"Yudan Wang, Liyuan Guo","doi":"10.3390/curroncol32030157","DOIUrl":null,"url":null,"abstract":"<p><p><b>Introduction:</b> Endometrial cancer (EC) is one of the most common gynecologic cancers, with an increasing incidence due to variables such as aging and lifestyle changes. Current biomarkers exhibit limited prognostic value, despite advancements in understanding their molecular basis, underscoring the necessity for new molecular markers. Microtubule affinity-regulating kinase 3 (MARK3) has been identified as a potential candidate owing to its established prognostic significance in various cancers; however, its function in endometrial cancer (EC) is not yet well understood. <b>Methods:</b> This study investigates the function of MARK3 in endometrial cancer through the analysis of Ishikawa and HEC-1B cell lines. A series of assays were conducted, including colony formation, CCK-8 viability, EDU proliferation assays, scratch wound healing tests, and Transwell migration assays, to investigate the effects of MARK3 overexpression. We conducted RT-qPCR, Western blot, and immunofluorescence assays to evaluate the molecular mechanisms influencing cell proliferation and migration. Bioinformatics analysis utilized publicly available datasets to examine the gene enrichment and co-expression networks. <b>Results:</b> The overexpression of MARK3 markedly reduced colony formation in both Ishikawa (<i>p</i> = 0.0039) and HEC-1B (<i>p</i> = 0.0014) cell lines. Furthermore, the overexpression of MARK3 led to decreased cell viability, as demonstrated by the EDU assay results (Ishikawa-OE <i>p</i> = 0.0302; HEC-OE <i>p</i> = 0.0037). The molecular analysis supported these findings, indicating an increase in phosphorylated AKT (pAKT), thereby suggesting MARK3's role in regulating cell survival pathways. Gene enrichment analysis revealed pathways associated with cell cycle regulation and apoptosis, whereas co-expression analysis pinpointed critical interacting genes that may play a role in EC progression. <b>Conclusions:</b> MARK3 is essential in the regulation of cell proliferation and migration in endometrial cancer, positioning it as a potential prognostic biomarker and therapeutic target. This study represents the inaugural investigation into the functional role of MARK3 in endothelial cell progression, thereby enhancing our comprehension of its mechanistic influence on cancer biology and its implications for personalized therapy. Bioinformatics analysis reinforces the relevance of MARK3 in endometrial cancer, offering new insights into its clinical significance.</p>","PeriodicalId":11012,"journal":{"name":"Current oncology","volume":"32 3","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941562/pdf/","citationCount":"0","resultStr":"{\"title\":\"Mark3 a Prognostic Marker for the Endometrial Cancer.\",\"authors\":\"Yudan Wang, Liyuan Guo\",\"doi\":\"10.3390/curroncol32030157\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b>Introduction:</b> Endometrial cancer (EC) is one of the most common gynecologic cancers, with an increasing incidence due to variables such as aging and lifestyle changes. Current biomarkers exhibit limited prognostic value, despite advancements in understanding their molecular basis, underscoring the necessity for new molecular markers. Microtubule affinity-regulating kinase 3 (MARK3) has been identified as a potential candidate owing to its established prognostic significance in various cancers; however, its function in endometrial cancer (EC) is not yet well understood. <b>Methods:</b> This study investigates the function of MARK3 in endometrial cancer through the analysis of Ishikawa and HEC-1B cell lines. A series of assays were conducted, including colony formation, CCK-8 viability, EDU proliferation assays, scratch wound healing tests, and Transwell migration assays, to investigate the effects of MARK3 overexpression. We conducted RT-qPCR, Western blot, and immunofluorescence assays to evaluate the molecular mechanisms influencing cell proliferation and migration. Bioinformatics analysis utilized publicly available datasets to examine the gene enrichment and co-expression networks. <b>Results:</b> The overexpression of MARK3 markedly reduced colony formation in both Ishikawa (<i>p</i> = 0.0039) and HEC-1B (<i>p</i> = 0.0014) cell lines. Furthermore, the overexpression of MARK3 led to decreased cell viability, as demonstrated by the EDU assay results (Ishikawa-OE <i>p</i> = 0.0302; HEC-OE <i>p</i> = 0.0037). The molecular analysis supported these findings, indicating an increase in phosphorylated AKT (pAKT), thereby suggesting MARK3's role in regulating cell survival pathways. Gene enrichment analysis revealed pathways associated with cell cycle regulation and apoptosis, whereas co-expression analysis pinpointed critical interacting genes that may play a role in EC progression. <b>Conclusions:</b> MARK3 is essential in the regulation of cell proliferation and migration in endometrial cancer, positioning it as a potential prognostic biomarker and therapeutic target. This study represents the inaugural investigation into the functional role of MARK3 in endothelial cell progression, thereby enhancing our comprehension of its mechanistic influence on cancer biology and its implications for personalized therapy. 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引用次数: 0
摘要
子宫内膜癌(EC)是最常见的妇科癌症之一,由于年龄和生活方式的改变等因素,发病率不断增加。尽管在了解其分子基础方面取得了进展,但目前的生物标志物显示出有限的预后价值,这强调了开发新的分子标志物的必要性。微管亲和调节激酶3 (MARK3)已被确定为潜在的候选者,因为它在各种癌症中具有确定的预后意义;然而,其在子宫内膜癌(EC)中的作用尚不清楚。方法:本研究通过石川细胞系和HEC-1B细胞系分析,探讨MARK3在子宫内膜癌中的功能。通过菌落形成、CCK-8活力、EDU增殖试验、划伤愈合试验和Transwell迁移试验等一系列试验来研究MARK3过表达的影响。我们通过RT-qPCR、Western blot和免疫荧光分析来评估影响细胞增殖和迁移的分子机制。生物信息学分析利用公开可用的数据集来检查基因富集和共表达网络。结果:过表达MARK3可显著减少Ishikawa细胞系(p = 0.0039)和HEC-1B细胞系(p = 0.0014)的集落形成。此外,EDU实验结果表明,MARK3过表达导致细胞活力下降(Ishikawa-OE p = 0.0302;HEC-OE p = 0.0037)。分子分析支持这些发现,表明磷酸化AKT (pAKT)增加,从而提示MARK3在调节细胞存活途径中的作用。基因富集分析揭示了与细胞周期调控和细胞凋亡相关的途径,而共表达分析指出了可能在EC进展中发挥作用的关键相互作用基因。结论:MARK3在子宫内膜癌细胞增殖和迁移的调控中起着至关重要的作用,是一种潜在的预后生物标志物和治疗靶点。这项研究首次研究了MARK3在内皮细胞进展中的功能作用,从而增强了我们对其对癌症生物学的机制影响及其对个性化治疗的影响的理解。生物信息学分析强化了MARK3在子宫内膜癌中的相关性,为其临床意义提供了新的见解。
Mark3 a Prognostic Marker for the Endometrial Cancer.
Introduction: Endometrial cancer (EC) is one of the most common gynecologic cancers, with an increasing incidence due to variables such as aging and lifestyle changes. Current biomarkers exhibit limited prognostic value, despite advancements in understanding their molecular basis, underscoring the necessity for new molecular markers. Microtubule affinity-regulating kinase 3 (MARK3) has been identified as a potential candidate owing to its established prognostic significance in various cancers; however, its function in endometrial cancer (EC) is not yet well understood. Methods: This study investigates the function of MARK3 in endometrial cancer through the analysis of Ishikawa and HEC-1B cell lines. A series of assays were conducted, including colony formation, CCK-8 viability, EDU proliferation assays, scratch wound healing tests, and Transwell migration assays, to investigate the effects of MARK3 overexpression. We conducted RT-qPCR, Western blot, and immunofluorescence assays to evaluate the molecular mechanisms influencing cell proliferation and migration. Bioinformatics analysis utilized publicly available datasets to examine the gene enrichment and co-expression networks. Results: The overexpression of MARK3 markedly reduced colony formation in both Ishikawa (p = 0.0039) and HEC-1B (p = 0.0014) cell lines. Furthermore, the overexpression of MARK3 led to decreased cell viability, as demonstrated by the EDU assay results (Ishikawa-OE p = 0.0302; HEC-OE p = 0.0037). The molecular analysis supported these findings, indicating an increase in phosphorylated AKT (pAKT), thereby suggesting MARK3's role in regulating cell survival pathways. Gene enrichment analysis revealed pathways associated with cell cycle regulation and apoptosis, whereas co-expression analysis pinpointed critical interacting genes that may play a role in EC progression. Conclusions: MARK3 is essential in the regulation of cell proliferation and migration in endometrial cancer, positioning it as a potential prognostic biomarker and therapeutic target. This study represents the inaugural investigation into the functional role of MARK3 in endothelial cell progression, thereby enhancing our comprehension of its mechanistic influence on cancer biology and its implications for personalized therapy. Bioinformatics analysis reinforces the relevance of MARK3 in endometrial cancer, offering new insights into its clinical significance.
期刊介绍:
Current Oncology is a peer-reviewed, Canadian-based and internationally respected journal. Current Oncology represents a multidisciplinary medium encompassing health care workers in the field of cancer therapy in Canada to report upon and to review progress in the management of this disease.
We encourage submissions from all fields of cancer medicine, including radiation oncology, surgical oncology, medical oncology, pediatric oncology, pathology, and cancer rehabilitation and survivorship. Articles published in the journal typically contain information that is relevant directly to clinical oncology practice, and have clear potential for application to the current or future practice of cancer medicine.