Translational Oncology最新文献

{"title":"FERMT1 promotes epithelial-mesenchymal transition of hepatocellular carcinoma by activating EGFR/AKT/β-catenin and EGFR/ERK pathways","authors":"","doi":"10.1016/j.tranon.2024.102144","DOIUrl":"10.1016/j.tranon.2024.102144","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to investigate the effects of fermitin family member 1 (FERMT1) on epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC) via the EGFR/AKT/β-catenin and EGFR/ERK pathways.</div></div><div><h3>Methods</h3><div>The expression of FERMT1 encoding protein kindlin-1 in HCC tissues was determined by immunohistochemistry, and FERMT1 mRNA expression in HCC tissues and cell lines was analyzed by qRT-PCR. After the FERMT1 expression of SNU182 and SNU387 interfered with siRNA, the cell viability, invasion, migration, and EMT were tested by CCK-8, transwell invasion, scratching, immunofluorescence/WB, respectively. Similarly, the effects of FERMT1 on the viability and metastasis of HCC were investigated in transplanted tumor and lung metastasis mouse models. The protein expressions of EGFR/AKT/β-catenin and EGFR/ERK pathways were analyzed by WB. In addition, the relationship between FERMT1 and EGFR was further determined by immunofluorescence double staining and Co-IP.</div></div><div><h3>Results</h3><div>FERMT1 was significantly upregulated in HCC, and silencing FERMT1 inhibited the viability, invasion, migration, and EMT of HCC. Silencing FERMT1 also inhibited the activation of EGFR/AKT/β-catenin and EGFR/ERK pathways. In addition, inhibition of EGFR, AKT, or ERK confirmed that EGFR/AKT/β-catenin and EGFR/ERK pathways were involved in the promoting effects of FERMT1 on HCC. Co-IP and immunofluorescence experiments confirmed the targeting relationship between FERMT1 and EGFR.</div></div><div><h3>Conclusion</h3><div>FERMT1 was highly expressed in HCC and promoted viability, invasion, migration, and EMT of HCC by targeting EGFR to activate the EGFR/AKT/β-catenin and EGFR/ERK pathways. Our study revealed the role of FERMT1 in HCC and suggested that FERMT1 exerts biological effects through activating the EGFR/AKT/β-catenin and EGFR/ERK pathways.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142359653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of LARP1B under endoplasmic reticulum stress and its regulatory role in proliferation of esophageal squamous cell carcinoma","authors":"","doi":"10.1016/j.tranon.2024.102141","DOIUrl":"10.1016/j.tranon.2024.102141","url":null,"abstract":"<div><div>Endoplasmic Reticulum Stress (ER stress) is a series of cellular responses activated in response to misfolded and unfolded protein accumulation and calcium imbalance in the ER lumen. Cumulating evidence emphasized the crucial involvement of ER stress in cell survival, death, and proliferation. However, the precise process remained obscure, especially in esophageal squamous cell carcinoma (ESCC). In the present study, LARP1B was detected to be one of the genes with significant differential expression in the ER stress ESCC cell model by RNA sequencing. ESCC cells exposed to ER stress stimulants (thapsigargin and tunicamycin) showed increased expression levels of LARP1B. ER stress initiated the expression of LARP1B through activation of the ERN1-XBP1 pathway, with XBP1 acting as a transcription factor to boost LARP1B transcription. Up-regulation of LARP1B was detected in ESCC tissues and cell lines. Suppression of LARP1B effectively curtailed the growth of cells and hindered the progression of the cell cycle. By detecting the expression of some genes closely related to proliferation and cell cycle regulation, CCND1 was identified as the main contributor to the cell proliferation induced by LARP1B. As an RNA-binding protein, LARP1B has the capability to attach to CCND1 mRNA, thereby increasing its stability. Inhibiting CCND1 might partially counterbalance the proliferation-promoting impact of LARP1B overexpression on ESCC cells. These findings indicate that, upon ER stress, up-regulation of LARP1B, triggered by ERN1-XBP1 pathway, facilitates proliferation of ESCC cells through enhancing the mRNA stability of CCND1, and LARP1B may be used as a potential therapeutic target of ESCC.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142327814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between URG4 and clinicopathologic parameters and its effect on two-year survival in gastric carcinoma","authors":"","doi":"10.1016/j.tranon.2024.102122","DOIUrl":"10.1016/j.tranon.2024.102122","url":null,"abstract":"<div><h3>Aim</h3><div>Gastric cancer (GC) is the third leading cause of cancer-related deaths worldwide. The present study examined the relationship between Upregulated gene 4 (URG4) expression, an oncogene involved in the development of gastric carcinoma, and clinicopathologic parameters including Human epidermal growth factor receptor 2 (HER2) status. The study aimed to investigate the importance of URG4 as a prognostic factor for 2-year survival in GCs, which are usually in the advanced stage at the time of diagnosis and have a rapid course.</div></div><div><h3>Methods</h3><div>In 61 patients with GC, URG4 expression results in paraffin blocks were compared with the patients' clinicopathologic, 2-year survival, and HER2 results.</div></div><div><h3>Results</h3><div>Among the patients, 24 (39 %) had low URG4 scores (scores 0–4) and 37 (61 %) had high URG4 scores (scores 6–9). While the HER2 score was negative in 52 (85 %)patients, it was positive in 9 (15 %). URG4 expression values were significantly correlated with tumor (T) stage and lymphovascular invasion (LVI) (<em>p</em> &lt; 0.005), whereas no significant correlation was determined between other pathological prognostic factors and HER2 status (<em>p</em> &gt; 0.005). During the two-year period, 32 (52 %) patients survived and 29 (48 %) died. The mean duration of survival was 75.20 ± 35.22 weeks. A significant correlation was determined between URG4 values and survival and mortality results (<em>p</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>We revealed a correlation (<em>p</em> &lt; 0.005) between increased URG4 scores with increased T stage and LVI. We demonstrated an association between increased URG4 expression and survival time and mortality in patients with GC during the first two years of survival (<em>p</em> &lt; 0.005) and URG4 and HER2 yielded similar results as prognostic factors in the survival of the patients URG4 is an essential oncogene in malignancies, especially in gastric GC, requiring further research and development in prognostic and therapeutic areas.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FHL2 activates β-catenin/Wnt signaling by complexing with APC and TRIM63 in lung adenocarcinoma","authors":"","doi":"10.1016/j.tranon.2024.102131","DOIUrl":"10.1016/j.tranon.2024.102131","url":null,"abstract":"<div><h3>Objectives</h3><div>Four and a half LIM domain 2 protein (FHL2) was reported to regulate the progression of various cancers and this study aimed to clarify the intrinsic mechanism of FHL2 facilitating the progression of lung adenocarcinoma.</div></div><div><h3>Methods</h3><div>In this study, bioinformatic analysis and immunohistochemistry staining were used to confirm the FHL2 levels in patients with lung adenocarcinoma. The potential influence of FHL2 on the biological function of lung adenocarcinoma cells was verified in vitro and in vivo. To uncover the potential mechanism contributing to the advance of lung adenocarcinoma, liquid chromatography‒mass spectrometry and immunoprecipitation assays were performed to detect the partners of FHL2.</div></div><div><h3>Results</h3><div>FHL2 levels were upregulated in lung adenocarcinoma and contributed to a dismal prognosis. Moreover, in vitro and in vivo assays suggested that genetic inhibition of FHL2 undermined the viability, migration and invasion of lung adenocarcinoma cells, while forced expression of FHL2 showed the opposite trend. Mechanistically, liquid chromatography‒mass spectrometry and coimmunoprecipitation assays revealed that FHL2 could function as a scaffold to enhance TRIM63-mediated ubiquitination of APC. The degradation of APC further stabilized β-catenin and activated Wnt signaling pathway.</div></div><div><h3>Conclusion</h3><div>Collectively, this study uncovered the underlying mechanism by which FHL2 regulates the biological characteristics of tumors and provided a novel target for lung adenocarcinoma treatment.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1936523324002584/pdfft?md5=76a9818eb0ecda2b1f964925fb7005c9&pid=1-s2.0-S1936523324002584-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142315103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-376a-3p sensitizes CPT-11-resistant colorectal cancer by enhancing apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) through the IGF1R/PI3K/AKT pathway","authors":"","doi":"10.1016/j.tranon.2024.102125","DOIUrl":"10.1016/j.tranon.2024.102125","url":null,"abstract":"<div><div>Colorectal cancer (CRC) remains the third most prevalent type of cancer worldwide contributing to an estimated 10 % of all cancer cases. CPT-11 is one of the first-line drugs for CRC treatment. Unfortunately, the development of drug resistance significantly exacerbates the adverse impact of CRC. Consequent tumor recurrences and metastasis, years after treatment are the frequently reported incidences. MicroRNAs (miRNA) are short non-coding RNA with the functionality of gene suppression. The insulin-like growth factor type 1 receptor (IGF1R) is a tyrosine kinase receptor frequently upregulated in cancers and is associated with cell survival and drug resistance. MiRNAs are frequently reported to be dysregulated in cancers including CRC. Evidence suggests that dysregulated miRNAs have direct consequences on the biological processes of their target genes. We previously demonstrated that miRNA-376a-3p is upregulated in CPT-11responsive, CRC cells upon treatment with CPT-11. We therefore aimed to investigate the involvement of miRNA-376a-3p in CPT-11 resistance and its probable association with IGF1R-mediated cancer cell survival. Our experimental approach used knockdown and overexpression experiments supplemented with western blot, RT-qPCR, flow cytometry, MTT, and migration assays to achieve our aim. Our data reveals the mechanism through which IGF1R and miRNA-376a-3p perpetrate and attenuate CPT-11 resistance respectively. MiRNA-376a-3p overexpression negatively regulated the IGF1R-induced cell survival, PI3K/AKT pathway, and reversed the epithelial-mesenchymal transition, hence sensitizing resistant cells to CPT-11. Our findings suggests that the miRNA-376a-3p/IGF1R axis holds promise as a potential target to sensitize CRC to CPT-11 in cases of drug resistance.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1936523324002523/pdfft?md5=cc1f8ffe40666f9a6ab8833d9fad58c2&pid=1-s2.0-S1936523324002523-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142311145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating exosomal protein EFEMP1 and SERPINC1 as diagnostic biomarkers for epithelial ovarian cancer","authors":"","doi":"10.1016/j.tranon.2024.102126","DOIUrl":"10.1016/j.tranon.2024.102126","url":null,"abstract":"<div><h3>Objectives</h3><div>Caner-derived exosomes, containing diverse nucleic acids and proteins, are being exploited in diagnostic biomarker development. This study aims to screen and identify the altered exosomal proteins between epithelial ovarian cancer (EOC) patient and healthy volunteers, and to evaluate their diagnostic accuracy for EOC.</div></div><div><h3>Methods</h3><div>Exosomes were separate by ultracentrifugation, and then subjected to TEM, qNano, and western blot for identification. Exosomal EFEMP1 and SERPINC1 were selected by MS/MS analysis, validated by ELISA in a cohort with 163 healthy donors, 183 EOC patients and 30 patients with benign ovarian tumors.</div></div><div><h3>Results</h3><div>MS/MS analyses identified a total of 207 differential exosomal proteins, including the 122 up-regulated and 85 down-regulated. Exosomal EFEMP1 and SERPINC1 were significantly upregulated in EOC patients compared with those in healthy donors as well as in the benign patients, possessing favorable diagnostic efficiency. The area under the curves (AUCs) were 0.8071, 0.8211, respectively. They also exerted rather high early diagnostic efficiency, as well as the potential to distinguish the malignant patients from the benign individuals. Besides, exosomal SERPINC1 was associated with coagulation index and LE-DVT (lower extremity deep venous thrombosis) in EOC patients.</div></div><div><h3>Conclusions</h3><div>Exosomal EFEMP1 and SERPINC1 are upregulated and serve as the promising diagnostic biomarkers for EOC.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1936523324002535/pdfft?md5=15f2b63b6468e058c3fe1bf8f7b90bc3&pid=1-s2.0-S1936523324002535-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142311253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the diagnostic utility of tRNA-derived fragments as biomarkers of head and neck cancer","authors":"","doi":"10.1016/j.tranon.2024.102135","DOIUrl":"10.1016/j.tranon.2024.102135","url":null,"abstract":"<div><div>Roughly 54,000 individuals are diagnosed with head and neck cancers in the United States yearly. Transfer RNA-derived fragments (tRF) are the products of enzymatic cleavage of precursor tRNAs, and have been proposed for use as biomarkers of head and neck cancer. In this study, we aim to further analyze the utility that tRFs might provide as biomarkers of head and neck cancer. tRF read counts were obtained for 453 tumor and 44 adjacent normal tissue samples and used to construct a gradient boosting diagnostic model. Although we identified 129 tRFs that were significantly dysregulated between these samples, the model achieved a sensitivity of only 69 % and a specificity of 59 %. tRFs are thought to induce the degradation of mRNA transcripts containing a complementary “seed” region. Despite the above performances, we chose to explore this concept of translational regulation by analyzing these tRFs for inverse correlation to the expression of select oncogenes and tumor suppressor genes implicated in head and neck cancer. Among others, CysGCA 5′-half and LysCTT 3′-tRF were upregulated in the tumor samples, and corresponded to decreased expression of PIK3R1, AKT1, and CPEB3. These transcripts were further found to contain numerous significantly complementary sites at which tRF-mediated mRNA degradation might occur. Although these tRFs did appear to correlate to many of the oncogenic metrics analyzed, we believe that additional research is needed before they might be used to improve the diagnosis, treatment, and survival of patients with this disease.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1936523324002626/pdfft?md5=25ef6d076bf2c33897667ed70e4a9523&pid=1-s2.0-S1936523324002626-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142311153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterisation of cells markers associated with IKZF1plus in BCP-ALL","authors":"","doi":"10.1016/j.tranon.2024.102127","DOIUrl":"10.1016/j.tranon.2024.102127","url":null,"abstract":"<div><div>The presence of <em>IKZF1</em> deletions has been associated with an increased relapse rate in B-cell precursor acute lymphoblastic leukaemia (BCP-ALL). There is a particular subset of <em>IKZF1</em>^del cases called <em>IKZF1</em>^plus (defined by the co-occurrence of <em>IKZF1</em>^del and deletions in <em>CDKN2A</em>/<em>B, PAX5</em>, or the PAR1 region, in the absence of <em>ERG</em> deletions), which is also associated with worse prognosis, but some recent studies have not found major differences between the <em>IKZF1</em>^del and <em>IKZF1</em>^plus groups. Therefore, the <em>IKZF1</em>^plus group still needs further comprehension and our study aims to characterise the molecular heterogeneity and identify molecular markers exclusively associated with <em>IKZF1</em>^plus. Two independent series of cases (TARGET, <em>n</em> = 125 and GenLAb, <em>n</em> = 60) were evaluated by segregating patients into 3 groups: <em>IKZF1</em>^plus, <em>IKZF1</em>^del, and <em>IKZF1</em>^wild. Differential expression analyses showed that the membrane protein-coding genes most associated with the <em>IKZF1</em>^plus group were: <em>KCNA5, GREB1, EPOR, SDK1</em>, and <em>PTPRB</em>. Notably, <em>KCNA5</em> and <em>GREB1</em> differential expression levels were validated in the GenLAb validation series. Regarding copy number alterations, we observed a high frequency of <em>VPREB1</em> deletions in the <em>IKZF1</em>^plus group, as well as additional exclusive deletions in the <em>CD200</em> and <em>BTLA</em> genes. Recent research suggests that the importance of the <em>IKZF1</em>^plus profile varies depending on the genetic subgroup. In this scenario, we found associations between <em>IKZF1</em>^plus and certain genes in BCP-ALL, being <em>KCNA5</em> and <em>GREB1</em> the most promising biomarkers for predicting <em>IKZF1</em>^plus. A deeper understanding of these genetic profiles will allow a better risk assessment and offer precise rationale for therapeutic strategies in BCP-ALL.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1936523324002547/pdfft?md5=280ef1d9a83a468a0730d31b6603c46d&pid=1-s2.0-S1936523324002547-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of hERG by ESEE suppresses the progression of colorectal cancer","authors":"","doi":"10.1016/j.tranon.2024.102137","DOIUrl":"10.1016/j.tranon.2024.102137","url":null,"abstract":"<div><p>Colorectal cancer (CRC) is one of the most common malignant cancers. Emodin is a lipophilic anthraquinone commonly found in medicinal herbs and known for its antitumor properties. However, its clinical utility has been hampered by low druggability. We designed and synthesized a new compound named Emodin succinimidyl ethyl ester (ESEE), which improves the bioavailability and preserves the original pharmacological effects of Emodin. In vitro, we have confirmed that ESEE induces apoptosis in colon cancer cells, suppresses cell proliferation, migration, and invasion, and inhibits the growth of subcutaneous transplantation tumors associated with colon cancer. And, in vivo, ESEE robustly inhibited tumor growth. Human Ether-a-go-go Related Gene (hERG) is aberrantly expressed in various cancer cells, where they play an important role in cancer progression. Focal adhesion kinase (FAK) is a tyrosine kinase overexpressed in cancer cells and plays an important role in the progression of tumors to a malignant phenotype. Mechanistically, the anti-CRC properties of ESEE are exerted through direct binding with hERG, which impedes the FAK/PI3K/AKT signaling axis-dependent apoptotic cascade.</p></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S193652332400264X/pdfft?md5=3b7225cf870c422e68d7f6a5a71eb27b&pid=1-s2.0-S193652332400264X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142270912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration of organoids in ovarian cancer: From basic research to clinical translation","authors":"","doi":"10.1016/j.tranon.2024.102130","DOIUrl":"10.1016/j.tranon.2024.102130","url":null,"abstract":"<div><p>Ovarian cancer is a highly heterogeneous tumor with a poor prognosis. The lack of reliable and efficient research models that can accurately mimic heterogeneity has impeded in-depth investigations and hindered the clinical translation of research findings in ovarian cancer. Organoid models have emerged as a promising in vitro approach, demonstrating remarkable fidelity to the histological, molecular, genomic, and transcriptomic features of their tissues of origin. In recent years, organoids have contributed to advancing our understanding of ovarian cancer initiation, metastasis, and drug resistance mechanisms, as well as facilitating clinical screening of effective therapeutic agents. The establishment of high-throughput organoid culture systems, coupled with cutting-edge technologies such as organ-on-a-chip, genetic engineering, and 3D printing, has tremendous potential for accelerating ovarian cancer research translation. In this review, we present a comprehensive overview of the latest exploration of organoids in basic ovarian cancer research and clinical translation. Furthermore, we discuss the prospects and challenges associated with the use of organoids and related novel technologies in the context of ovarian cancer. This review provides insights into the application of organoids in ovarian cancer.</p></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1936523324002572/pdfft?md5=3ea2118734dadcbeb8994ff489911d17&pid=1-s2.0-S1936523324002572-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142270985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}