Ovarian cancer (OvCa) develops asymptomatically until it reaches the advanced stages with metastasis, chemoresistance, and poor prognosis. Our review focuses on the analysis of regulatory long non-coding RNAs (lncRNAs) competing with protein-coding mRNAs for binding to miRNAs according to the model of competitive endogenous RNA (ceRNA) in OvCa. Analysis of publications showed that most lncRNAs acting as ceRNAs participate in OvCa progression: migration, invasion, epithelial-mesenchymal transition (EMT), and metastasis. More than 30 lncRNAs turned out to be predictors of survival and/or response to therapy in patients with OvCa. For a number of oncogenic (CCAT1, HOTAIR, NEAT1, and TUG1 among others) and some suppressive lncRNAs, several lncRNA/miRNA/mRNA axes were identified, which revealed various functions for each of them. Our review also considers examples of alternative mechanisms of actions for lncRNAs besides being ceRNAs, including binding directly to mRNA or protein, and some of them (DANCR, GAS5, MALAT1, and UCA1 among others) act by both mechanisms depending on the target protein. A systematic analysis based on the data from literature and Panther or KEGG (Kyoto Encyclopedia of Genes and Genomes) databases showed that a significant part of lncRNAs affects the key pathways involved in OvCa metastasis, EMT, and chemoresistance.

https://www.mdpi.com/1422-0067/21/22/8855/pdf

LncRNAs in Ovarian Cancer Progression, Metastasis, and Main Pathways: ceRNA and Alternative Mechanisms.

Increased intracellular toxicity due to an imbalance in copper homeostasis caused by copper ion accumulation could regulate the rate of cancer cell growth and proliferation. The goal of this study was to create a novel Cuproptosis-related lncRNA signature that may be utilized to predict survival and immunotherapy in HCC patients. Cuproptosis-associated lncRNAs and differentially expressed lncRNAs between HCC tumor tissue and normal tissue were discovered first. By LASSO-Cox analysis, the overlapping lncRNAs were then utilized to build a Cuproptosis-associated lncRNA signature, which might be used to predict patient prognosis and responsiveness to immune checkpoint blockade (ICB) therapy. Differences in the infiltration of immune cell subpopulations between high and low-risk score subgroups were also analyzed. Moreover, a nomogram based on the Cuproptosis-associated lncRNA signature and clinical features was developed and demonstrated to have good predictive potential. Finally, qRT-PCR was performed in HerpG2 and MHCC-97H cell lines to explore whether these lncRNAs were indeed involved in the process of Cuproptosis. In summary, we created a prognostic lncRNA profile linked to Cuproptosis to forecast response to immunotherapy, which may provide a new potential non-apoptotic therapeutic perspective for HCC patients. 

/pdf/a-novel-cuproptosis-related-lncrna-signature-to-predict-3edne0f3.pdf

A novel Cuproptosis-related LncRNA signature to predict prognosis in hepatocellular carcinoma

Abstract Cancer ranks as one of the deadliest diseases worldwide. The high mortality rate associated with cancer is partially due to the lack of reliable early detection methods and/or inaccurate diagnostic tools such as certain protein biomarkers. Cell-free nucleic acids (cfNA) such as circulating long noncoding RNAs (lncRNAs) have been proposed as a new class of potential biomarkers for cancer diagnosis. The reported correlation between the presence of tumors and abnormal levels of lncRNAs in the blood of cancer patients has notably triggered a worldwide interest among clinicians and oncologists who have been actively investigating their potentials as reliable cancer biomarkers. In this report, we review the progress achieved (“the Good”) and challenges encountered (“the Bad”) in the development of circulating lncRNAs as potential biomarkers for early cancer diagnosis. We report and discuss the diagnostic performance of more than 50 different circulating lncRNAs and emphasize their numerous potential clinical applications (“the Beauty”) including therapeutic targets and agents, on top of diagnostic and prognostic capabilities. This review also summarizes the best methods of investigation and provides useful guidelines for clinicians and scientists who desire conducting their own clinical studies on circulating lncRNAs in cancer patients via RT-qPCR or Next Generation Sequencing (NGS). 

/pdf/blood-derived-lncrnas-as-biomarkers-for-cancer-diagnosis-the-22ecttb1.pdf

Blood-derived lncRNAs as biomarkers for cancer diagnosis: the Good, the Bad and the Beauty

Oral squamous cell carcinoma (OSCC) ranks as the sixth most common carcinoma worldwide, and the third most common carcinoma in developing countries as well. Recently, the aberrant expression of lncRNA CCAT1 has been revealed to play an important role in the development of several cancers. However, its role in OSCC remains unknown. The expression levels of CCAT1 and miR-181a were determined in 15 paired primary OSCC tissues and their adjacent noncancerous tissues and cell lines with qPCR. shRNA against CCAT1 was employed to investigate the impact of CCAT1 on proliferation and metastasis. Then dual luciferase reporter and RIP assays were utilized to study the interaction between CCAT1 and miR-181a. Cells transfected with sh-CCAT1 or treated with miR-181a inhibitor were subjected to western blot to investigate the role of Wnt/β-catenin signaling in CCAT1-mediated proliferation and metastasis. Finally, the role of CCAT1 in OSCC was confirmed with tumor xenografts mice model. CCAT1 was upregulated in OSCC tissues and cell lines. Knockdown of CCAT1 inhibited the proliferation, migration and invasion of OSCC cells, while the cell apoptosis was enhanced. Luciferase and RIP assays revealed that miR-181a was a direct target of CCAT1. Inhibition of miR-181a partially reversed the efficacy of sh-CCAT1. Moreover, sh-CCAT1 inhibited OSCC tissues growth through inhibiting Wnt signaling in a miR-181a-dependent manner in vivo. lncRNA CCAT1 activated Wnt/β-catenin signaling via inhibiting miR-181a, resulting in the cell proliferation, migration and invasion of OSCC, suggesting that CCAT1 might serve as a potential target of OSCC treatment. Abbreviation: LncRNA: long non-coding RNA; OSCC: oral squamous cell carcinoma; 3' UTR: 3' untranslated region; ANOVA: one-way analysis of variance; CDK: cyclin-dependent kinase; ceRNA: competing endogenous RNA; FBS: fetal bovine serum; HGF: human gingival fibroblasts; MAPK: mitogen-activated protein kinase; miRNA: micro RNA; ncRNA: noncoding RNAs; PBS: phosphate-buffered saline; PI3K: phosphatidylinositol 3-kinase.

Long non-coding RNA CCAT1 is a prognostic biomarker for the progression of oral squamous cell carcinoma via miR-181a-mediated Wnt/β-catenin signaling pathway.

Ovarian cancer is one of the most lethal gynecological malignancies worldwide because it tends to be detected late, when the disease has already spread, and prognosis is poor. In this review we aim to highlight the importance of long non-coding RNAs (lncRNAs) in diagnosis, prognosis and treatment choice, to make progress towards increasingly personalized medicine in this malignancy. We review the effects of lncRNAs associated with ovarian cancer in the context of cancer hallmarks. We also discuss the molecular mechanisms by which lncRNAs become involved in cellular physiology; the onset, development and progression of ovarian cancer; and lncRNAs' regulatory mechanisms at the transcriptional, post-transcriptional and post-translational stages of gene expression. Finally, we compile a series of online resources useful for the study of lncRNAs, especially in the context of ovarian cancer. Future work required in the field is also discussed along with some concluding remarks.

https://www.mdpi.com/2072-6694/12/4/1020/pdf

The Challenges and Opportunities of LncRNAs in Ovarian Cancer Research and Clinical Use

Objective To explore whether lncRNA GIHCG participates in the pathogenic progression of ovarian cancer (OC) and its underlying mechanism. Patients and methods Expression levels of GIHCG and microRNA-429 in 30 OC tissues and normal ovarian tissues were detected by quantitative Real time-polymerase chain reaction (qRT-PCR). Subsequently, 15 pairs of OC tissues and paracancerous tissues were selected for correlation analyses of GIHCG, microRNA-429 and the overall survival (OS) of OC patients using Kaplan-Meier method. Pearson correlation analyses were conducted for investigating the correlation between GIHCG and microRNA-429. GIHCG expression in OC cell lines (HEY, A2780 and HO8910) and normal epithelial OC cell line (IOSE-386) was detected by qRT-PCR. After transfection of GIHCG overexpression plasmid in HEY cells, cell cycle, proliferation and colony formation ability were detected by flow cytometry, cell counting kit-8 (CCK-8) and colony formation assay. MicroRNA-429 expression in HEY cells overexpressing GIHCG was detected by qRT-PCR. Rescue experiments were conducted by co-transfection of GIHCG overexpression plasmid and microRNA-429 mimics, followed by cell cycle and colony formation detection. Results GIHCG was highly expressed, whereas microRNA-429 was lowly expressed in OC tissues than that of paracancerous tissues. OC patients with higher expression of GIHCG showed shorter OS than those with lower expression. However, OC patients with higher expression of microRNA-429 had longer OS than those with lower expression. GIHCG expression was positively correlated to microRNA-429. In vitro experiments showed that GIHCG was highly expressed in HEY, A2780 and HO8910 cells than that of IOSE-386 cells. GIHCG overexpression in HEY cells promoted cell cycle and colony formation abilities, which were reversed by microRNA-429 overexpression. Conclusions GIHCG is highly expressed in OC, which promotes OC development by stimulating cell cycle progression and cell proliferation by regulating microRNA-429.

LncRNA GIHCG promotes development of ovarian cancer by regulating microRNA-429.

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LncRNA GIHCG promotes development of ovarian cancer by regulating microRNA-429.