Molecular Carcinogenesis最新文献_第3页

Interferon-Inducible ADAR1 p150 Is Essential for the Survival of Oral Squamous Cell Carcinoma. 干扰素诱导的ADAR1 p150对口腔鳞状细胞癌的生存至关重要。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-26 DOI: 10.1002/mc.23910

Pei San Yee, Annie Wai Yeeng Chai, Shi Mun Yee, Shiyin Ooi, Yee Hua Tan, Mathew J Garnett, Siew Kit Ng, Sok Ching Cheong

{"title":"Interferon-Inducible ADAR1 p150 Is Essential for the Survival of Oral Squamous Cell Carcinoma.","authors":"Pei San Yee, Annie Wai Yeeng Chai, Shi Mun Yee, Shiyin Ooi, Yee Hua Tan, Mathew J Garnett, Siew Kit Ng, Sok Ching Cheong","doi":"10.1002/mc.23910","DOIUrl":"https://doi.org/10.1002/mc.23910","url":null,"abstract":"We identified ADAR1 as one of the top essential genes for oral squamous cell carcinoma (OSCC) survival from our genome-wide CRISPR/Cas9 screen in OSCC cell lines. In this study, we confirm that ADAR1-knockout (KO) inhibits cell viability and colony forming ability, and induces apoptosis. We report that IFN-β treatment sensitizes less-dependent cell lines to ADAR1 KO-induced cell lethality. Overexpression of ADAR1-p150, but not ADAR1-p110, rescued cell lethality upon ADAR1 KO, confirming that the IFN-inducible p150 is responsible for OSCC survival. Using a deaminase inactive mutant, we demonstrate that the editing function of ADAR1 is important for OSCC survival. Furthermore, we show that ADAR1 KO-induced cell death is mediated by both PKR and MDA5. We compute gene signatures of ADAR1 dependency in OSCC tumors, and found that those with high ADAR1 dependency score are associated with well or moderate differentiation, likely due to high PKR expression or activation. While a majority of ADAR1-dependent tumors exhibit a low T cell-inflamed gene expression profile, ADAR1 KO upregulates PD-L1, a marker of anti-PD1 response, indicating that ADAR1 inhibition may enhance immunotherapy response in OSCC. Collectively, these findings suggest that targeting ADAR1-p150 not only induces OSCC cell death but could induce a favorable response to anti-PD1.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SOAT1 Activates NLRP3 Inflammasome to Promote Cancer-Related Lymphangiogenesis and Metastasis via IL-1β/IL-1R-1 Axis in Oral Squamous Cell Carcinoma. SOAT1激活NLRP3炎性体，通过IL-1β/IL-1R-1轴促进口腔鳞状细胞癌相关淋巴管生成和转移

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-26 DOI: 10.1002/mc.23907

Chengzhi Zhao, Yuhao Wang, Zhishen Jiang, Shengzhao Guo, Liru Hu, Jian Pan, Fan Dan

{"title":"SOAT1 Activates NLRP3 Inflammasome to Promote Cancer-Related Lymphangiogenesis and Metastasis via IL-1β/IL-1R-1 Axis in Oral Squamous Cell Carcinoma.","authors":"Chengzhi Zhao, Yuhao Wang, Zhishen Jiang, Shengzhao Guo, Liru Hu, Jian Pan, Fan Dan","doi":"10.1002/mc.23907","DOIUrl":"https://doi.org/10.1002/mc.23907","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) is a prevalent type of cancer in the head and neck region, significantly impacting patient survival rates and quality of life. Lymph node (LN) metastasis is a lead contributor to the poor prognosis associated with OSCC. SOAT1 plays a critical role in cholesterol metabolism and has been implicated in various cancers, although its specific mechanisms in OSCC are poorly understood. Additionally, NLRP3 inflammasome has been identified as a factor that promotes cancer progression by influencing various processes involved in tumor development, with its activation linked to cancer metastasis. Lymphangiogenesis enhancing cancer metastasis has been identified in OSCC, while the molecule networks of regulating it remains unclear. In our study, we found that SOAT1 is overexpressed in OSCC and promotes proliferation, migration, and invasion of OSCC cells. Knockdown SOAT1 expression impaired OSCC progression both in vitro and in vivo, and reduced the rate of LN metastasis. RNA sequencing analysis revealed that NLRP3 is a downstream regulated by SOAT1, with NLRP3 inflammasome reactivation having recovered cancer malignancy inhibited by SOAT1 knockdown. Furthermore, we revealed that IL-1β, released by NLRP3 inflammasome activation, could directly bind to IL-1R-1 in lymphatic endothelial cells (LECs), and enhance tube formation capacity of LECs, indicating the potential role of NLRP3 inflammasome in promoting lymphangiogenesis and metastasis in OSCC. In conclusion, SOAT1 could promote OSCC malignancy and regulate the activation of NLRP3 inflammasome to increase the rate of lymphangiogenesis and cancer metastasis via IL-1β/IL-1R-1 axis in OSCC.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GPR87 Promotes Angiogenesis in Esophageal Squamous Cell Carcinoma via VEGFA Regulation. GPR87通过VEGFA调控促进食管鳞状细胞癌血管生成。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-26 DOI: 10.1002/mc.23909

Dengyan Zhu, Donglei Liu, Kai Wu, Xingdong Cheng, Yang Yang

{"title":"GPR87 Promotes Angiogenesis in Esophageal Squamous Cell Carcinoma via VEGFA Regulation.","authors":"Dengyan Zhu, Donglei Liu, Kai Wu, Xingdong Cheng, Yang Yang","doi":"10.1002/mc.23909","DOIUrl":"https://doi.org/10.1002/mc.23909","url":null,"abstract":"The role and underlying mechanisms of G protein-coupled receptor 87 (GPR87) in esophageal squamous cell carcinoma (ESCC) remain unclear, despite its established oncogenic functions in other malignancies. This study examined the expression of GPR87 and its association with survival rate in ESCC using online databases. The expression of GPR87 in ESCC tissues was identified using immunohistochemistry, and a correlation analysis was carried out using ki-67 data. ESCC cells were transfected with GPR87 knockdown or overexpression plasmids, followed by functional assays such as, CCK-8 for cell viability, colony formation for proliferation, wound healing for migration, Transwell for invasion, and tube formation for angiogenesis. Western blot analysis was used to assess STAT3 phosphorylation and VEGFA expression. Additionally, a xenograft tumor model was established to investigate the effect of GPR87 on tumor growth in vivo. The findings demonstrated that GPR87 was highly expressed in ESCC tissues and its overexpression was associated with a poor patient survival. Transfection with a GPR87 overexpression plasmid increases the cell viability, invasion, proliferation, and angiogenesis of ESCC cells, while transfection with sh-GPR87 reversed these effects. Additionally, GPR87 controlled VEGFA expression levels by promoting STAT3 phosphorylation. Rescue trials further verified that GPR87 promotes the growth of ESCC by modulating STAT3. Moreover, in vivo studies validated that GPR87 knockdown suppressed tumor growth. In conclusion, the findings highlight GPR87 as a key regulator of VEGFA expression via STAT3 activation, contributing to ESCC malignancy. Targeting GPR87 may provide a potential therapeutic strategy for ESCC.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hsa_circ_0000231 Accelerates Cell Autophagy and Promotes Cell Proliferation and Invasion of Colorectal Cancer via miR-140-3p/Bcl-2 Axis. Hsa_circ_0000231通过miR-140-3p/Bcl-2轴加速细胞自噬，促进结直肠癌细胞增殖和侵袭。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-26 DOI: 10.1002/mc.23906

Long Zhao, Haoran Zhang, Shuo Wang, Yushi Zhou, Kewei Jiang, Shan Wang, Yingjiang Ye, Bo Wang, Zhanlong Shen

{"title":"Hsa_circ_0000231 Accelerates Cell Autophagy and Promotes Cell Proliferation and Invasion of Colorectal Cancer via miR-140-3p/Bcl-2 Axis.","authors":"Long Zhao, Haoran Zhang, Shuo Wang, Yushi Zhou, Kewei Jiang, Shan Wang, Yingjiang Ye, Bo Wang, Zhanlong Shen","doi":"10.1002/mc.23906","DOIUrl":"https://doi.org/10.1002/mc.23906","url":null,"abstract":"Accumulating evidence indicated that circular RNAs (circRNAs) directly sponge to microRNAs (miRNAs),(miRNAs), which in turn regulate the gene expression and affect the malignancy behavior at the posttranscriptional level. However, the expression levels, function, and mechanism of circ_0000231 in colorectal cancer (CRC) are largely unknown. The expression levels of circ_0000231, miR-140-3p, and Bcl-2 in 110 CRC tissues and matched normal colorectal tissues were detected by qRT-PCR method. circ_0000231 and Bcl-2 were suppressed by siRNA, and miR-140-3p was overexpressed by RNA mimics in CRC cell lines. The function-based experiments were conducted to detect the proliferation and migratory abilities in CRC cell lines. RNA pull-down, RNA immunoprecipitation (RIP), and dual-fluorescence reporter assay were conducted to verify the association among circ_0000231, miR-140-3p, and Bcl-2. Western blot analysis and mRFP-GFP-LC3 adenovirus were used to detect the autophagy level affected by circ_0000231, miR-140-3p, and Bcl-2 axis. Downregulated circ_0000231 significantly suppressed the proliferation and migratory abilities of CRC cells by suppressing autophagy and promoting G0/G1 phase arrest. Furthermore, RNA pull-down, RIP, and dual-fluorescence reporter assays confirmed that circ_0000231 regulates the expression of Bcl-2 by directly targeting miR-140-3p. More importantly, circ_0000231 promoted the levels of autophagy via the miR-140-3p/Bcl-2 axis in CRC. Our study demonstrated that circ_0000231, as a tumor promotor, enhances the level of autophagy by regulating Bcl-2 via targeting miR-140-3p. Moreover, circ_0000231 might serve as a diagnostic and prognostic indicator and a novel molecular target for CRC therapy.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

C1QBP Promotes Prostate Cancer Progression and Lipid Accumulation by Negatively Regulating ALDH9A1. C1QBP通过负调控ALDH9A1促进前列腺癌进展和脂质积累。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23904

Xinyu Liu, Jiaxin Li, Runxuan Du, Qiufang Qiao, Shuang Liu, Zhihao Bo, Ruibing Chen, Yihan Dong, Xuesong Xiao, Yuejing Pan, Huamao Jiang, Rui Wang, Yong Wang, Dan Yue

{"title":"C1QBP Promotes Prostate Cancer Progression and Lipid Accumulation by Negatively Regulating ALDH9A1.","authors":"Xinyu Liu, Jiaxin Li, Runxuan Du, Qiufang Qiao, Shuang Liu, Zhihao Bo, Ruibing Chen, Yihan Dong, Xuesong Xiao, Yuejing Pan, Huamao Jiang, Rui Wang, Yong Wang, Dan Yue","doi":"10.1002/mc.23904","DOIUrl":"https://doi.org/10.1002/mc.23904","url":null,"abstract":"Prostate cancer (PCa) relies heavily on lipid metabolism for energy acquisition, and lipid metabolic reprogramming plays a crucial role in its progression. Here, we utilized publicly available PCa databases and immunohistochemistry to evaluate C1QBP expression in PCa. We found that C1QBP is highly expressed in PCa, potentially due to promoter hypomethylation. Functional assays showed that C1QBP promotes cell proliferation, migration, and lipid accumulation in PCa cells. We identified differentially expressed proteins associated with C1QBP by using liquid chromatography-tandem mass spectrometry. Functional enrichment analysis revealed that C1QBP affects lipid metabolism and negatively regulates the lipid metabolism-related molecule ALDH9A1. Furthermore, ALDH9A1 intervention rescued the tumor suppression and lipid reduction caused by C1QBP knockdown. RNA sequencing (RNA-seq) was performed to explore C1QBP regulatory pathways at the mRNA level, revealing that C1QBP also affects the MAPK and p53 pathways, as well as the expression of lipid metabolism-related molecules. In conclusion, these findings suggest that C1QBP influences PCa progression and lipid deposition by regulating ALDH9A1, while other potential mechanisms may also be involved, indicating that C1QBP is a promising target for PCa treatment.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells. CtBP2通过EGR1调控Wnt信号影响DLBCL细胞的增殖和凋亡

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23901

Jianfang Dong, Lihua Li, Xuefei Zhang, Xijing Yin, Zucong Chen

{"title":"CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.","authors":"Jianfang Dong, Lihua Li, Xuefei Zhang, Xijing Yin, Zucong Chen","doi":"10.1002/mc.23901","DOIUrl":"https://doi.org/10.1002/mc.23901","url":null,"abstract":"Diffuse large B-cell lymphoma (DLBCL) is the most prevalent form of lymphoma. The overexpression of CtBP2 in tissues may contribute to tumor occurrence and progression. The expression of EGR1 in DLBCL is elevated, suggesting its potential role as an oncogene that promotes the proliferation of DLBCL cells. Database predictions indicate that CtBP2 can bind to EGR1. The objective of the present study was to investigate whether CtBP2 can influence the proliferation and apoptosis of DLBCL cells by regulating the Wnt signaling pathway through EGR1. Western blot assay showed that CtBP2 expression was upregulated in DLBCL cells. Cell proliferation level was detected by CCK8 assay and EdU staining, and the apoptosis level and cycle distribution were analyzed through flow cytometry. Our data indicated that interference with CtBP2 and EGR1 can inhibit the proliferation and cell cycle progression of DLBCL cells while promoting apoptosis. The predictions from the HDOCK server, along with the results of Co-IP experiments, suggested that EGR1 and CtBP2 can effectively bind to each other, with EGR1 positioned downstream of CtBP2 and regulated by it. Furthermore, interference with CtBP2 could also inhibit the expression of the Wnt/β-catenin signaling pathway. Overexpression of EGR1 counteracted the effects of siRNA-CtBP2, promoting cell proliferation and cycle, inhibiting apoptosis and upregulating the expression of the Wnt/β-catenin signaling pathway. From the above experiments, we found that CtBP2 can regulate the Wnt/β-catenin signaling pathway through EGR1 to influence the proliferation and apoptosis of DLBCL cells. Therefore, EGR1 may be one of the key contributors involved in the regulation of Wnt/β-catenin signaling by CtBP2.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

P21-Activated Kinase 1 (PAK1) Modulates Therapeutic Response to Ionizing Radiation in Head and Neck Squamous Cell Carcinoma Cells. p21活化激酶1 （PAK1）调节头颈部鳞状细胞癌细胞对电离辐射的治疗反应。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23902

Swetha Rajendran, Rohan Prasad Surabhi, A Satheesh Kumar, Prarthana Gopinath, Vishnupriya Kanakaveti, Gouthaman Shanmugasundaram, M Michael Gromiha, Suresh Kumar Rayala, Ganesh Venkatraman

{"title":"P21-Activated Kinase 1 (PAK1) Modulates Therapeutic Response to Ionizing Radiation in Head and Neck Squamous Cell Carcinoma Cells.","authors":"Swetha Rajendran, Rohan Prasad Surabhi, A Satheesh Kumar, Prarthana Gopinath, Vishnupriya Kanakaveti, Gouthaman Shanmugasundaram, M Michael Gromiha, Suresh Kumar Rayala, Ganesh Venkatraman","doi":"10.1002/mc.23902","DOIUrl":"https://doi.org/10.1002/mc.23902","url":null,"abstract":"Head and neck squamous cell carcinoma (HNSCC) continues to be a formidable epithelial malignancy characterized by late-stage detection and recurrence impacting survival. P21-activated kinase-1 (PAK1) was reported to be overexpressed in head and neck cancers and activated by ionizing radiation (IR), affecting treatment outcomes. Present investigations revealed that PAK1 silencing on HNSCC cells reverted the aggressive phenotype and showed impaired DNA damage repair upon IR exposure. Further HNSCC cells were resistant to IR up to 30 Gy with elevated pPAK1 levels. Radiation-resistant (RR) HNSCC cells expressed radiation-resistant markers, namely MRE-11 and NME-1; stemness markers-OCT4 and SOX2; and EMT & metastasis markers-vimentin, snail, and α-smooth muscle actin (α-SMA). In addition, HNSCC RR cells showed increased levels of DNA damage response protein H2AX, indicative of an aggressive phenotype with an augmented DNA repair machinery and a potential target for inhibition. Since H2AX appears to be a mechanistic hub for PAK1-induced radiation resistance, using in silico methods, peptides were designed, and the PL-8 peptide was chosen to target the phosphorylation of H2AX, which could enhance the sensitivity to IR and push the cells to radiation-induced cell death. PL-8 peptide inhibited H2AX phosphorylation on HNSCC cells and triggered radiation-induced cell death as determined by functional assays. The present study reveals PAK1 induced in HNSCC cells by IR and causes resistance by enhancing DNA damage response mediated through γH2AX. To counteract this complex molecular interplay, we propose inhibiting γH2AX formation & silencing PAK1 appears to be a probable way forward in HNSCC.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circ_0044362 Facilitates the Progression of Epithelial Ovarian Cancer via Enhancing HOXB4 Transcription to Activate the RUNX1/IGFBP3 Axis. Circ_0044362通过增强HOXB4转录激活RUNX1/IGFBP3轴促进上皮性卵巢癌的进展。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23905

Shengtou Ye, Han Wu, Junjiang Liu, Jianguo Zhou, Sisi He, Na Li

{"title":"Circ_0044362 Facilitates the Progression of Epithelial Ovarian Cancer via Enhancing HOXB4 Transcription to Activate the RUNX1/IGFBP3 Axis.","authors":"Shengtou Ye, Han Wu, Junjiang Liu, Jianguo Zhou, Sisi He, Na Li","doi":"10.1002/mc.23905","DOIUrl":"https://doi.org/10.1002/mc.23905","url":null,"abstract":"Increasing numbers of studies have elucidated the emerging roles of circular RNA (circRNA) in cancer progression. However, the function of circRNAs in modulating their parental genes in ovarian cancer remains poorly understood. In this study, we identified that circ_0044362, a circRNA derived from homeobox B4 (HOXB4), significantly promotes the expression of its parental gene HOXB4 in ovarian cancer. Functionally, circ_0044362 promotes the malignant phenotypes of ovarian cancer cells. Further analysis revealed that circ_0044362 facilitates the transcriptional activation of its parental gene HOXB4 by directly guiding U1 small nuclear ribonucleoprotein (snRNP) to its promoter region, thereby enhancing the oncogenic behaviors of ovarian cancer cells. Furthermore, HOXB4 positively regulates runt-related transcription factor 1 (RUNX1) expression, with RUNX1 serving as a transcription factor to promote the transcription of insulin-like growth factor binding protein-3 (IGFBP3). Notably, inhibitors of either HOXB4, RUNX1, or IGFBP3 could reverse the oncogenic activity mediated by circ_0044362. Collectively, our findings reveal the involvement of the circ_0044362/HOXB4 pathway in ovarian cancer progression and provide potential therapeutic strategies for ovarian cancer treatment.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LINC02154 Promotes Esophageal Squamous Cell Carcinoma Progression via the PI3K-AKT-mTOR Signaling Pathway by Interacting With IGF2BP2. LINC02154通过PI3K-AKT-mTOR信号通路与IGF2BP2相互作用促进食管鳞状细胞癌进展

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23903

Mingyuan Zhang, Cai Zhang, Fuyou Zhou, Ruotong Yang, Yang Feng, Yangyang Ji, Huijun Ren, Liang Ming

引用次数: 0

Correction to "Plasma DNA Methylation-Based Biomarkers for MPNST Detection in Patients With Neurofibromatosis Type 1". 修正“血浆DNA甲基化生物标志物用于1型神经纤维瘤病患者MPNST检测”。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23890

引用次数: 0