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HSPB8-BAG3 chaperone complex modulates cell invasion in intrahepatic cholangiocarcinoma by regulating CASA-mediated Filamin A degradation. HSPB8-BAG3伴侣复合物通过调节CASA介导的Filamin A降解来调节肝内胆管癌的细胞侵袭。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-08-31 DOI: 10.1080/15384047.2024.2396694
Bo Shu, Yu Wen, Ronghua Lin, Chao He, Cailan Luo, Fazhao Li

The incidence of intrahepatic cholangiocarcinoma (ICC) is steadily rising, and it is associated with a high mortality rate. Clinical samples were collected to detect the expression of HSPB8 and BAG3 in ICC tissues. ICC cells were cultured and transfected with plasmids that overexpressed or silenced specific genes to investigate the impact of gene expression alterations on cell function. qPCR and Western blot techniques were utilized to measure gene and protein expression levels. A wound healing assay was conducted to assess cell migration ability. The Transwell assay was used to assess cell invasion ability. Co-IP was used to verify the binding relationship between HSPB8 and BAG3. The effects of HSPB8 and BAG3 on lung metastasis of tumors in vivo were verified by constructing a metastatic tumor model. Through the above experiments, we discovered that the expressions of HSPB8 and BAG3 were up-regulated in ICC tissues and cells, and their expressions were positively correlated. The metastatic ability of ICC cells could be promoted or inhibited by upregulating or downregulating the expression of BAG3. Furthermore, the HSPB8-BAG3 chaperone complex resulted in the abnormal degradation of Filamin A by activating autophagy. Increased expression of Filamin A inhibits the migration and invasion of ICC cells. Overexpression of HSPB8 and BAG3 in vivo promoted the lung metastasis ability of ICC cells. The HSPB8-BAG3 chaperone complex promotes ICC cell migration and invasion by regulating CASA-mediated degradation of Filamin A, offering insights for enhancing ICC therapeutic strategies.

肝内胆管癌(ICC)的发病率正在稳步上升,而且死亡率很高。我们收集了临床样本,以检测 ICC 组织中 HSPB8 和 BAG3 的表达。培养 ICC 细胞并用过表达或沉默特定基因的质粒进行转染,以研究基因表达改变对细胞功能的影响。伤口愈合试验用于评估细胞迁移能力。Transwell 试验用于评估细胞侵袭能力。Co-IP 用于验证 HSPB8 和 BAG3 之间的结合关系。通过构建转移性肿瘤模型,验证了 HSPB8 和 BAG3 对体内肿瘤肺转移的影响。通过上述实验,我们发现HSPB8和BAG3在ICC组织和细胞中表达上调,且两者的表达呈正相关。通过上调或下调BAG3的表达,可以促进或抑制ICC细胞的转移能力。此外,HSPB8-BAG3伴侣复合物通过激活自噬作用导致Filamin A异常降解。Filamin A的表达增加会抑制ICC细胞的迁移和侵袭。在体内过表达HSPB8和BAG3可促进ICC细胞的肺转移能力。HSPB8-BAG3伴侣复合物通过调节CASA介导的Filamin A降解促进了ICC细胞的迁移和侵袭,为加强ICC治疗策略提供了启示。
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引用次数: 0
Tripartite motif-containing protein 50 suppresses triple-negative breast cancer progression by regulating the epithelial-mesenchymal transition. 含三方基序蛋白 50 通过调节上皮-间充质转化抑制三阴性乳腺癌的进展。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-11-13 DOI: 10.1080/15384047.2024.2427410
Danxiang Chen, Jing Jiang, Wei Zhang, Xinlin Li, Qidong Ge, Xia Liu, Xujun Li

Background and objectives: Tripartite motif-containing protein 50 (TRIM50) is a recently discovered E3 ubiquitin ligase that participates in tumor progression. TRIM50 is overexpressed in many cancers, although few studies focused on TRIM50's role in breast cancer.

Methods: We overexpressed TRIM50 in triple-negative breast cancer cell lines using plasmid and found that TRIM50 upregulation markedly reduced breast cancer cell proliferation, clone formation, and migration, as well as promoted breast cancer cell apoptosis. Western blotting revealed that accumulated TRIM50 resulted in both mRNA and protein depletion of SNAI1, and partially attenuated the epithelial-mesenchymal transition (EMT) induced by SNAI1.

Results: In this study, we demonstrate that TRIM50 is downregulated in human breast cancer and that its overexpression closely correlates with diminished invasion capacity in breast cancer, suggesting that TRIM50 may serve as a diagnostic marker and therapeutic target.

Conclusion: TRIM50 plays a key role in breast cancer proliferation and potentially serves as a prognostic and therapeutic target.

背景和目的:含三方基序蛋白 50(TRIM50)是最近发现的一种参与肿瘤进展的 E3 泛素连接酶。TRIM50在许多癌症中都有过表达,但很少有研究关注TRIM50在乳腺癌中的作用:我们利用质粒在三阴性乳腺癌细胞系中过表达了TRIM50,发现TRIM50的上调明显减少了乳腺癌细胞的增殖、克隆形成和迁移,并促进了乳腺癌细胞的凋亡。Western印迹显示,TRIM50的积累会导致SNAI1的mRNA和蛋白消耗,并部分减轻SNAI1诱导的上皮-间质转化(EMT):本研究表明,TRIM50在人类乳腺癌中下调,其过表达与乳腺癌侵袭能力的减弱密切相关,这表明TRIM50可作为诊断标志物和治疗靶点:结论:TRIM50 在乳腺癌增殖过程中起着关键作用,有可能成为预后和治疗的靶点。
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引用次数: 0
The critical role of tumor microbiome in cancer immunotherapy. 肿瘤微生物组在癌症免疫疗法中的关键作用。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-01-19 DOI: 10.1080/15384047.2024.2301801
Liu Yang, Qi Wang, Lijuan He, Xingyu Sun

In recent years, the microbiome has shown an integral role in cancer immunotherapy and has become a prominent and widely studied topic. A full understanding of the interactions between the tumor microbiome and various immunotherapies offers opportunities for immunotherapy of cancer. This review scrutinizes the composition of the tumor microbiome, the mechanism of microbial immune regulation, the influence of tumor microorganisms on tumor metastasis, and the interaction between tumor microorganisms and immunotherapy. In addition, this review also summarizes the challenges and opportunities of immunotherapy through tumor microbes, as well as the prospects and directions for future related research. In conclusion, the potential of microbial immunotherapy to enhance treatment outcomes for cancer patients should not be underestimated. Through this review, it is hoped that more research on tumor microbial immunotherapy will be done to better solve the treatment problems of cancer patients.

近年来,微生物组在癌症免疫疗法中显示出不可或缺的作用,并已成为一个突出和广泛研究的课题。充分了解肿瘤微生物组与各种免疫疗法之间的相互作用为癌症免疫疗法提供了机遇。本综述仔细研究了肿瘤微生物组的组成、微生物免疫调节的机制、肿瘤微生物对肿瘤转移的影响以及肿瘤微生物与免疫疗法之间的相互作用。此外,本综述还总结了通过肿瘤微生物进行免疫治疗所面临的挑战和机遇,以及未来相关研究的前景和方向。总之,微生物免疫疗法在提高癌症患者治疗效果方面的潜力不容小觑。通过本综述,希望能有更多关于肿瘤微生物免疫疗法的研究,以更好地解决癌症患者的治疗问题。
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引用次数: 0
The predictors of lymphopenia and its effects on survival in locally advanced esophageal squamous cell carcinoma. 局部晚期食管鳞状细胞癌淋巴细胞减少的预测因素及其对生存期的影响。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-07-01 DOI: 10.1080/15384047.2024.2371632
Danjing Luo, Qiulu Zhong, Haiying Yue, Jue Wang, Qianfu Liang, Wenqi Liu, Xiaodong Zhu

To investigate the impact of the effective radiation dose to immune cells (EDIC) and gross tumor volume (GTV) on lymphopenia and survival in patients with locally advanced esophageal squamous cell carcinoma (LAESCC). Between January 2013 and December 2020, 272 LAESCC patients were treated with definitive radiotherapy in two institutions. Based on radiation doses to the lungs, heart, and body region scanned, EDIC was calculated as an equal uniform dose to the total blood considering blood flow and fraction effect. The radiotherapy plan was used to calculate the GTVs. Lymphopenia was graded based on the lowest lymphocyte count during RT. The overall survival (OS), progress-free survival (PFS), and local recurrence-free survival (LRFS) were analyzed statistically. The lowest lymphocyte count was significantly correlated with EDIC (r= -0.389, p < .001) and GTV (r= -0.211, p < .001). Lymphopenia, EDIC, and GTV are risk factors for patients with ESCC. In a Kaplan-Meier analysis with EDIC and GTV as stratification factors, lymphopenia was not associated with OS in the EDIC>12.9 Gy group (p = .294)and EDIC ≤ 12.9 Gy group, and it was also not associated with OS in GTV>68.8 cm3 group (p = .242) and GTV ≤ 68.8 cm3 group(p = .165). GTV and EDIC had an impact on the relationship between lymphopenia and OS in patients with LAESCC undergoing definitive RT. Poorer OS, PFS, and LRFS are correlated with lymphopenia, higher EDIC, and larger GTV.

研究免疫细胞有效辐射剂量(EDIC)和肿瘤总体积(GTV)对局部晚期食管鳞状细胞癌(LAESCC)患者淋巴细胞减少症和生存期的影响。2013年1月至2020年12月期间,两家机构共对272名LAESCC患者进行了确定性放疗。根据肺部、心脏和身体扫描区域的辐射剂量,考虑到血流量和分数效应,EDIC被计算为总血液中的等量均匀剂量。放疗计划用于计算GTV。淋巴细胞减少症根据放疗期间的最低淋巴细胞计数进行分级。对总生存期(OS)、无进展生存期(PFS)和无局部复发生存期(LRFS)进行了统计分析。最低淋巴细胞计数与 EDIC(r= -0.389,p < .001)和 GTV(r= -0.211,p < .001)显著相关。淋巴细胞减少症、EDIC和GTV是ESCC患者的危险因素。在以EDIC和GTV为分层因素的Kaplan-Meier分析中,淋巴细胞减少与EDIC>12.9 Gy组(p = .294)和EDIC≤12.9 Gy组的OS无关,与GTV>68.8 cm3组(p = .242)和GTV≤68.8 cm3组(p = .165)的OS也无关。GTV和EDIC对接受确定性RT治疗的LAESCC患者淋巴细胞减少与OS之间的关系有影响。较差的OS、PFS和LRFS与淋巴细胞减少、较高的EDIC和较大的GTV相关。
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引用次数: 0
Evaluating massage therapy for radiation-induced fibrosis in rats: preliminary findings and palpation results.
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-12-02 DOI: 10.1080/15384047.2024.2436694
Geoffrey M Bove, Holly McMillan, Mary F Barbe

Radiation-induced fibrosis (RIF) is a common side effect of cancer treatment, but can manifest into a devastating syndrome for which there is no preventive measure or cure. In rats who perform a repetitive work task, who left untreated develop signs and symptoms that resemble repetitive motion disorders in humans, we have shown that manual therapy prevents the development of fibrosis and other key biomarkers. The fibrosis of RIF and repetitive motion disorders has similar biomarkers. In rats, we sought to determine if manual therapy would alter key biomarkers of post-irradiation fibrosis following X-ray irradiation given to the rat forelimb. One limb of rats was given a damaging dose of X-ray irradiation. Some limbs were massaged using a protocol previously described and characterized. Serum inflammatory markers, histological assays of tissue fibrosis and nerve pathology, and electrophysiology for neuropathic discharge were assayed after 8 weeks. We also tested if an experienced therapist could identify the irradiated limb using blinded palpation at the 8 week end-point. While preliminary assays showed robust changes compared to control limbs, the other assays did not show similar pathology. Our therapist could detect each irradiated limb. Serum inflammatory markers were reduced by massage to the irradiated limb. We conclude that blinded palpation is sensitive to detect subtle changes in tissue following irradiation. In contrast to the preliminary studies, the dose of irradiation used was insufficient to induce long-lasting deep fibrosis or nerve degeneration. We suspect that a difference in housing, and thus physical activity, was the plausible reason for this difference.

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引用次数: 0
Navigating precision: the crucial role of next-generation sequencing recurrence risk assessment in tailoring adjuvant therapy for hormone receptor-positive, human epidermal growth factor Receptor2-negative early breast cancer. 精准导航:下一代测序复发风险评估在为激素受体阳性、人类表皮生长因子受体2阴性的早期乳腺癌量身定制辅助治疗中的关键作用。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-09-20 DOI: 10.1080/15384047.2024.2405060
Ying Xu, Yingxue Qi, Zhongyu Lu, Yuan Tan, Dongsheng Chen, Haijun Luo

Hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) breast cancer is the most common subtype, representing over two-thirds of new diagnoses. Adjuvant therapy, which encompasses various medications and treatment durations, is the standard approach for managing early stage HR+ HER2- breast cancer. Optimizing treatment is essential to minimize unnecessary side effects while addressing the biological variability inherent in HR+/HER2- breast cancers. Incorporating biological biomarkers into treatment decisions, alongside traditional clinical factors, is vital. Gene expression assays can identify patients unlikely to benefit from adjuvant chemotherapy, thereby refining treatment strategies and improving risk assessment. This paper reviews evidence for several genomic tests, including Oncotype DX, MammaPrint, Breast Cancer Index, RucurIndex, and EndoPredict, which assist in tailoring adjuvant therapy. Additionally, we explore the role of liquid biopsies in personalizing treatment, emphasizing the importance of considering late relapse risks and potential benefits of extended systemic therapy for HR+/HER2- breast cancer patients.

激素受体阳性(HR+)/人表皮生长因子受体 2 阴性(HER2-)乳腺癌是最常见的亚型,占新诊断病例的三分之二以上。辅助治疗包括各种药物和治疗持续时间,是治疗早期 HR+ HER2-乳腺癌的标准方法。优化治疗对于最大限度地减少不必要的副作用,同时解决HR+/HER2-乳腺癌固有的生物学变异性至关重要。将生物标志物与传统临床因素一起纳入治疗决策至关重要。基因表达检测可以确定不太可能从辅助化疗中获益的患者,从而完善治疗策略并改进风险评估。本文回顾了几种基因组检测的证据,包括 Oncotype DX、MammaPrint、Breast Cancer Index、RucurIndex 和 EndoPredict,这些检测有助于调整辅助治疗。此外,我们还探讨了液体活检在个性化治疗中的作用,强调了考虑HR+/HER2-乳腺癌患者晚期复发风险和延长系统治疗的潜在益处的重要性。
{"title":"Navigating precision: the crucial role of next-generation sequencing recurrence risk assessment in tailoring adjuvant therapy for hormone receptor-positive, human epidermal growth factor Receptor2-negative early breast cancer.","authors":"Ying Xu, Yingxue Qi, Zhongyu Lu, Yuan Tan, Dongsheng Chen, Haijun Luo","doi":"10.1080/15384047.2024.2405060","DOIUrl":"10.1080/15384047.2024.2405060","url":null,"abstract":"<p><p>Hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2-) breast cancer is the most common subtype, representing over two-thirds of new diagnoses. Adjuvant therapy, which encompasses various medications and treatment durations, is the standard approach for managing early stage HR+ HER2- breast cancer. Optimizing treatment is essential to minimize unnecessary side effects while addressing the biological variability inherent in HR+/HER2- breast cancers. Incorporating biological biomarkers into treatment decisions, alongside traditional clinical factors, is vital. Gene expression assays can identify patients unlikely to benefit from adjuvant chemotherapy, thereby refining treatment strategies and improving risk assessment. This paper reviews evidence for several genomic tests, including Oncotype DX, MammaPrint, Breast Cancer Index, RucurIndex, and EndoPredict, which assist in tailoring adjuvant therapy. Additionally, we explore the role of liquid biopsies in personalizing treatment, emphasizing the importance of considering late relapse risks and potential benefits of extended systemic therapy for HR+/HER2- breast cancer patients.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2405060"},"PeriodicalIF":4.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11418226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
S-1-based concurrent chemoradiotherapy plus nimotuzumab in patients with locally advanced esophageal squamous cell carcinoma who failed neoadjuvant therapy: a real-world prospective study. 对新辅助治疗失败的局部晚期食管鳞癌患者进行基于S-1的同步化放疗加尼莫妥珠单抗治疗:一项真实世界的前瞻性研究。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-10-27 DOI: 10.1080/15384047.2024.2417464
Xin Wang, Guojie Feng, Xiongtao Yang, Nuo Yu, Ziyu Zheng, Jiao Li, Xiaozheng Kang, Xiankai Chen, Ruixiang Zhang, Yong Li, Zhen Wang, Lei Deng, Tao Zhang, Wenyang Liu, Jianyang Wang, Wenqing Wang, Qinfu Feng, Zefen Xiao, Zongmei Zhou, Nan Bi, Yin Li, Jianjun Qin

Purpose: This prospective study in a real-world setting investigated the feasibility and safety of S-1 plus nimotuzumab (S-1-Nimo) based concurrent chemoradiotherapy (CCRT) in locally advanced esophageal squamous cell carcinoma (LA-ESCC) patients who failed to neoadjuvant chemotherapy or chemoimmunotherapy.

Methods: LA-ESCC patients who failed to converse to resectable disease after neoadjuvant chemotherapy or chemoimmunotherapy were enrolled to receive the 4-week S-1-Nimo regimen of radiotherapy (40 Gy in 20 fractions, 5 days per week), S-1 chemotherapy, and nimotuzumab. Then, after surgical assessments, patients evaluated as resectable disease received surgery; patients with unresectable disease continued to receive definitive radiotherapy (50-60 Gy in 25-30 fractions, 5 days per week) concurrently with S-1-Nimo. The primary endpoint was event-free survival (EFS).

Results: Sixty-four patients were enrolled and evaluated. The median follow-up time was 23.2 months. Median EFS was 9.6 (95% confidence interval [CI], 7.1-14.0) months, with an estimated 2-year EFS rate of 24.2%. The median overall survival (OS) and the estimated OS rate at 2 years were 13.4 (95% CI, 10.3-17.5) months and 31.2%, respectively. Twelve underwent surgery, with a surgical conversion rate of 18.8% and an R0 resection rate of 100.0%. Subgroup analysis identified the significantly prolonged EFS and OS in patients who experienced radical surgery (median EFS, not reached vs. 8.7 months; p = .0117. median OS, 24.9 vs. 10.6 months; p = .0205) as compared to those treated with CCRT. Of 64 patients, grade 3 adverse events mainly included radiation esophagitis (4.7%), anemia (1.6%), and thrombocytopenia (1.6%).

Conclusion: The study demonstrated the reasonable efficacy and promising safety of the S-1-Nimo-based CCRT in LA-ESCC patients with failure to neoadjuvant chemotherapy or chemoimmunotherapy.

目的:这项前瞻性研究在真实世界环境中调查了基于S-1加尼莫妥珠单抗(S-1-Nimo)的同步化学放疗(CCRT)在新辅助化疗或化学免疫治疗失败的局部晚期食管鳞状细胞癌(LA-ESCC)患者中的可行性和安全性:新辅助化疗或化疗免疫治疗失败的局部晚期食管鳞癌(LA-ESCC)患者入组,接受为期4周的S-1-Nimo方案放疗(40 Gy,20次/分,每周5天)、S-1化疗和尼莫妥珠单抗治疗。然后,在手术评估后,被评估为可切除疾病的患者接受手术治疗;不可切除疾病的患者在接受S-1-尼莫治疗的同时继续接受确定性放疗(50-60 Gy,分25-30次,每周5天)。主要终点是无事件生存期(EFS):结果:64 名患者接受了治疗和评估。中位随访时间为 23.2 个月。中位无事件生存期为 9.6 个月(95% 置信区间 [CI],7.1-14.0),估计 2 年无事件生存率为 24.2%。中位总生存期(OS)和预计2年OS率分别为13.4个月(95% CI,10.3-17.5)和31.2%。12例患者接受了手术治疗,手术转化率为18.8%,R0切除率为100.0%。亚组分析发现,与接受CCRT治疗的患者相比,接受根治性手术的患者的EFS和OS明显延长(中位EFS,未达8.7个月 vs. 8.7个月;p = .0117;中位OS,24.9个月 vs. 10.6个月;p = .0205)。64名患者中,3级不良事件主要包括放射性食管炎(4.7%)、贫血(1.6%)和血小板减少(1.6%):该研究表明,在新辅助化疗或化疗免疫治疗失败的LA-ESCC患者中,基于S-1-尼莫的CCRT具有合理的疗效和良好的安全性。
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引用次数: 0
Expression and clinical significance of NLRC5 in hepatocellular carcinoma. 肝细胞癌中 NLRC5 的表达和临床意义。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-08-12 DOI: 10.1080/15384047.2024.2390205
Xiangyu Ma, Shangkun Ning, Tong Sun, Mei Liu, Jibing Liu

NLRC5, the largest member of the nucleotide-binding and oligomerization domain (NOD)-like receptor (NLR) family, has been reported to participate in the regulation of immune function and is associated with chronic inflammatory diseases. However, the biological function of NLRC5 in hepatocellular carcinoma (HCC) has not been fully demonstrated. The aim of this study is to evaluate NLRC5 expression in the tumor tissues of HCC patients undergoing surgical treatment, assess its prognostic value, and explore its relationship with critical immune-related molecules within the tumor microenvironment. A total of 100 patients with hepatitis B virus-associated HCC receiving surgical treatment were enrolled in the study. Immunohistochemical results were obtained by scoring the intensity of cellular staining and the percentage of positive cells in the tissue sections. The association between NLRC5 expression levels and the main clinicopathological factors was analyzed by Chi-square test method. The prognostic values were analyzed by COX regression model and the Kaplan-Meier survival curve. Receiver operating characteristic (ROC) curve analysis was performed to assess the predictive performance of NLRC5 in postoperative patients with HCC. IHC showed that high expression of NLRC5 was observed in 67% of HCC tissue samples. Chi-square test showed that NLRC5 was a risk factor associated with tumor number, satellite nodule, and envelope invasion. Kaplan-Meier survival curves and COX survival analysis showed that high expression of NLRC5 was significantly associated with decreased overall survival (OS) in HCC patients (HR = 1.79, 95% CI 1.03-3.12, p = .041). However, univariate logistic regression analysis revealed that NLRC5 showed positive relationship with GZMB and CD8α suggesting its role in immune escape of HCC. ROC curve analysis showed that the combination of tumor number, envelope invasion, and NLRC5 expression (area under the curve = 0.824, sensitivity = 77.30%, specificity = 82.4%) can more accurately evaluate the prognosis of HCC patients compared to the combination of only tumor number and envelope invasion (area under the curve = 0.690, sensitivity = 43.9%, specificity = 94.1%).NLRC5 plays a crucial role in progression of HCC and can be considered as a potential prognostic and predictive biomarker. Targeting NLRC5 may provide an attractive therapeutic approach for HCC.

NLRC5是核苷酸结合和寡聚化结构域(NOD)样受体(NLR)家族中最大的成员,据报道它参与调节免疫功能,并与慢性炎症性疾病相关。然而,NLRC5 在肝细胞癌(HCC)中的生物学功能尚未得到充分证实。本研究旨在评估接受手术治疗的 HCC 患者肿瘤组织中 NLRC5 的表达,评估其预后价值,并探讨其与肿瘤微环境中关键免疫相关分子的关系。研究共纳入了100名接受手术治疗的乙肝病毒相关性HCC患者。通过对组织切片中的细胞染色强度和阳性细胞百分比进行评分,得出免疫组化结果。NLRC5表达水平与主要临床病理因素之间的关系采用Chi-square检验法进行分析。预后值通过 COX 回归模型和 Kaplan-Meier 生存曲线进行分析。为评估 NLRC5 对术后 HCC 患者的预测能力,进行了接收者操作特征(ROC)曲线分析。IHC显示,在67%的HCC组织样本中观察到NLRC5的高表达。卡普兰-梅耶生存曲线(Kaplan-Meier survival curve)显示,NLRC5是与肿瘤数量、卫星结节和包膜侵犯相关的风险因素。卡普兰-梅耶生存曲线和 COX 生存分析表明,NLRC5 的高表达与 HCC 患者总生存期(OS)的降低显著相关(HR = 1.79,95% CI 1.03-3.12,p = .041)。然而,单变量逻辑回归分析显示,NLRC5与GZMB和CD8α呈正相关,表明其在HCC免疫逃逸中的作用。ROC曲线分析表明,肿瘤数目、包膜侵犯和NLRC5表达的组合(曲线下面积=0.824,灵敏度=77.30%,特异度=82.4%)与仅有肿瘤数目和包膜侵犯的组合(曲线下面积=0.690,灵敏度=43.9%,特异度=94.1%)相比,能更准确地评估HCC患者的预后。靶向 NLRC5 可为 HCC 提供一种有吸引力的治疗方法。
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引用次数: 0
POLE2 silencing inhibits the progression of colorectal carcinoma cells via wnt signaling axis. 沉默 POLE2 可通过 wnt 信号轴抑制结直肠癌细胞的进展。
IF 4.4 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-08-18 DOI: 10.1080/15384047.2024.2392339
Weihua Jian, Lei Zhang

Colorectal cancer (CRC) is one of the most common malignant carcinoma worldwide. DNA polymerase epsilon 2, accessory subunit (POLE2) participates in DNA replication, repair, and cell cycle control, but its association with CRC development remains unclear. In the present study, the differentially expressed genes (DEGs) in CRC were screened from bioinformatics analysis based on GEO database. RT-qPCR was used to assess mRNA expression. CCK-8 and colony formation assays were applied for the evaluation of cell proliferation. Wound healing and transwell assays were used to detect cell migration and invasion. Protein levels were determined by Western blotting assay. We found that POLE2 was highly expressed in CRC tissues and cell lines. Inhibition of POLE2 suppressed the proliferation, migration and invasion of CRC cells. Mechanistically, Wnt/β-catenin signaling pathway was inactivated by inhibition of POLE2. Activation of Wnt/β-catenin pathway can reverse the function of POLE2 knockdown on CRC cells. In vivo studies demonstrated that POLE2 silencing could notably inhibit the growth of tumors, which was consistent with the results in vitro. In conclusion, we found POLE2 as a novel oncogene in CRC, providing a potential therapeutic or diagnostic target in CRC.

结直肠癌(CRC)是全球最常见的恶性肿瘤之一。DNA 聚合酶ε2附属亚基(POLE2)参与DNA复制、修复和细胞周期控制,但它与CRC发病的关系仍不清楚。本研究以 GEO 数据库为基础,通过生物信息学分析筛选出 CRC 中的差异表达基因(DEGs)。采用 RT-qPCR 评估 mRNA 表达。CCK-8和集落形成试验用于评估细胞增殖。伤口愈合和透孔试验用于检测细胞迁移和侵袭。蛋白水平则通过 Western 印迹检测来确定。我们发现 POLE2 在 CRC 组织和细胞系中高表达。抑制 POLE2 可抑制 CRC 细胞的增殖、迁移和侵袭。从机制上讲,POLE2抑制了Wnt/β-catenin信号通路的失活。激活 Wnt/β-catenin 通路可以逆转 POLE2 敲除对 CRC 细胞的作用。体内研究表明,POLE2沉默能显著抑制肿瘤的生长,这与体外研究结果一致。总之,我们发现 POLE2 是 CRC 中的一种新型癌基因,为 CRC 提供了一个潜在的治疗或诊断靶点。
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引用次数: 0
Correction. 更正。
IF 3.6 4区 医学 Q2 ONCOLOGY Pub Date : 2024-12-31 Epub Date: 2024-02-13 DOI: 10.1080/15384047.2024.2318833
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引用次数: 0
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Cancer Biology & Therapy
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