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doi:10.18632/oncotarget.v8i27

Cited by 13 publications

(6 citation statements)

References 5 publications

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“…This was achieved by upregulating the expression of PCK1. Further findings indicated that hsa_circ_0005986 functioned as a tumor suppressor in the progression of HCC (286). The expression of hsa_circ_0005986 was significantly downregulated in HCC tissues compared to healthy tissues.…”

Section: An Overview Of Circrnas In Cancermentioning

confidence: 85%

Exploring non-coding RNA mechanisms in hepatocellular carcinoma: implications for therapy and prognosis

Tian,

Zhang,

Liu

et al. 2024

Front. Immunol.

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Hepatocellular carcinoma (HCC) is a significant contributor to cancer-related deaths in the world. The development and progression of HCC are closely correlated with the abnormal regulation of non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). Important biological pathways in cancer biology, such as cell proliferation, death, and metastasis, are impacted by these ncRNAs, which modulate gene expression. The abnormal expression of non-coding RNAs in HCC raises the possibility that they could be applied as new biomarkers for diagnosis, prognosis, and treatment targets. Furthermore, by controlling the expression of cancer-related genes, miRNAs can function as either tumor suppressors or oncogenes. On the other hand, lncRNAs play a role in the advancement of cancer by interacting with other molecules within the cell, which, in turn, affects processes such as chromatin remodeling, transcription, and post-transcriptional processes. The importance of ncRNA-driven regulatory systems in HCC is being highlighted by current research, which sheds light on tumor behavior and therapy response. This research highlights the great potential of ncRNAs to improve patient outcomes in this difficult disease landscape by augmenting the present methods of HCC care through the use of precision medicine approaches.

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Section: An Overview Of Circrnas In Cancermentioning

confidence: 85%

Exploring non-coding RNA mechanisms in hepatocellular carcinoma: implications for therapy and prognosis

Tian,

Zhang,

Liu

et al. 2024

Front. Immunol.

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“…EPCAM has been widely studied as a therapeutic target and a prognostic marker in various epithelial malignancies, including breast, ovarian, urothelial, and non-small cell lung carcinomas. Tayama et al found that high EPCAM levels correlated with chemotherapy resistance and poor prognosis in ovarian cancer patients; thus, targeting EPCAM is a potential promising approach to treat chemoresistant ovarian cancer 77. However, data from Woopen et al showed that EPCAM overexpression in EOC was significantly associated with improved OS ( P = 0.015) and an increased rate of response to platinum-based chemotherapy ( P = 0.048) 78.…”

Section: Discussionmentioning

confidence: 99%

<p>Integrated Analysis To Identify Molecular Biomarkers Of High-Grade Serous Ovarian Cancer</p>

Si¹,

Zhang²,

Cao³

et al. 2019

OTT

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PurposeOvarian cancer is the leading cause of gynecologic cancer-related death worldwide. Early diagnosis of ovarian cancer can significantly improve patient prognosis. Hence, there is an urgent need to identify key diagnostic and prognostic biomarkers specific for ovarian cancer. Because high-grade serous ovarian cancer (HGSOC) is the most common type of ovarian cancer and accounts for the majority of deaths, we identified potential biomarkers for the early diagnosis and prognosis of HGSOC.MethodsSix datasets (GSE14001, GSE18520, GSE26712, GSE27651, GSE40595, and GSE54388) were downloaded from the Gene Expression Omnibus database for analysis. Differentially expressed genes (DEGs) between HGSOC and normal ovarian surface epithelium samples were screened via integrated analysis. Hub genes were identified by analyzing protein–protein interaction (PPI) network data. The online Kaplan-Meier plotter was utilized to evaluate the prognostic roles of these hub genes. The expression of these hub genes was confirmed with Oncomine datasets and validated by quantitative real-time PCR and Western blotting.ResultsA total of 103 DEGs in patients with HGSOC—28 upregulated genes and 75 downregulated genes—were successfully screened. Enrichment analyses revealed that the upregulated genes were enriched in cell division and cell proliferation and that the downregulated genes mainly participated in the Wnt signaling pathway and various metabolic processes. Ten hub genes were associated with HGSOC pathogenesis. Seven overexpressed hub genes were partitioned into module 1 of the PPI network, which was enriched in the cell cycle and DNA replication pathways. Survival analysis revealed that MELK, CEP55 and KDR expression levels were significantly correlated with the overall survival of HGSOC patients (P < 0.05). The RNA and protein expression levels of these hub genes were validated experimentally.ConclusionBased on an integrated analysis, we propose the further investigation of MELK, CEP55 and KDR as promising diagnostic and prognostic biomarkers of HGSOC.

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“…Basic research identifying the role of the cyclin D-CDK4/6-Rb axis in G1 to S cell cycle transit, followed by translational and clinical studies in which this axis was linked to breast cancer progression and antiestrogen resistance ( 46 , 47 ), culminated in the development of CDKi’s currently used in combination with endocrine treatments for ER + HER2 negative breast cancer ( 48 ). CDK4/6 small molecule inhibitors currently used as an adjuvant to antiestrogen treatment include palbociclib, ribociclib, and abemaciclib.…”

Section: Cdki As An Adjuvant To Antiestrogen Therapymentioning

confidence: 99%

Autophagy and senescence facilitate the development of antiestrogen resistance in ER positive breast cancer

McGrath,

Abolhassani,

Guy

et al. 2024

Front. Endocrinol.

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Estrogen receptor positive (ER+) breast cancer is the most common breast cancer diagnosed annually in the US with endocrine-based therapy as standard-of-care for this breast cancer subtype. Endocrine therapy includes treatment with antiestrogens, such as selective estrogen receptor modulators (SERMs), selective estrogen receptor downregulators (SERDs), and aromatase inhibitors (AIs). Despite the appreciable remission achievable with these treatments, a substantial cohort of women will experience primary tumor recurrence, subsequent metastasis, and eventual death due to their disease. In these cases, the breast cancer cells have become resistant to endocrine therapy, with endocrine resistance identified as the major obstacle to the medical oncologist and patient. To combat the development of endocrine resistance, the treatment options for ER+, HER2 negative breast cancer now include CDK4/6 inhibitors used as adjuvants to antiestrogen treatment. In addition to the dysregulated activity of CDK4/6, a plethora of genetic and biochemical mechanisms have been identified that contribute to endocrine resistance. These mechanisms, which have been identified by lab-based studies utilizing appropriate cell and animal models of breast cancer, and by clinical studies in which gene expression profiles identify candidate endocrine resistance genes, are the subject of this review. In addition, we will discuss molecular targeting strategies now utilized in conjunction with endocrine therapy to combat the development of resistance or target resistant breast cancer cells. Of approaches currently being explored to improve endocrine treatment efficacy and patient outcome, two adaptive cell survival mechanisms, autophagy, and “reversible” senescence, are considered molecular targets. Autophagy and/or senescence induction have been identified in response to most antiestrogen treatments currently being used for the treatment of ER+ breast cancer and are often induced in response to CDK4/6 inhibitors. Unfortunately, effective strategies to target these cell survival pathways have not yet been successfully developed. Thus, there is an urgent need for the continued interrogation of autophagy and “reversible” senescence in clinically relevant breast cancer models with the long-term goal of identifying new molecular targets for improved treatment of ER+ breast cancer.

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Abstract: News on: Sphingosine kinase 2 inhibition synergises with bortezomib to target myeloma by enhancing endoplasmic reticulum stressby Wallington-Beddoe et al.

Cited by 13 publications

References 5 publications

Exploring non-coding RNA mechanisms in hepatocellular carcinoma: implications for therapy and prognosis

Exploring non-coding RNA mechanisms in hepatocellular carcinoma: implications for therapy and prognosis

<p>Integrated Analysis To Identify Molecular Biomarkers Of High-Grade Serous Ovarian Cancer</p>

Autophagy and senescence facilitate the development of antiestrogen resistance in ER positive breast cancer

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