Long non-coding RNAs in recurrent ovarian cancer: Theranostic perspectives

Bhardwaj, Vipul; Tan, Yan Qin; Wu, Ming; Ma, Liang; Zhu, Tao; Lobie, Peter E.; Pandey, Vijay

doi:10.1016/j.canlet.2020.12.042

Cited by 21 publications

(12 citation statements)

References 132 publications

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“…Recent studies have shown that lncRNAs, which are stable non-coding RNAs greater than 200, can act as upstream regulators by binding and regulating specific miRNAs involved in various biological processes, including tumor cell proliferation, apoptosis, invasion and metastasis [ 18 ]. Many lncRNAs have considerable tissue or cell type specificity [ 19 ], and lncRNAs as a new participant play in the initiation, maintenance and progression of tumourigenesis [ 7 , 20 ]. For example, like lncrna differentiation against non proteins coding RNA (DANCR) plays a promotional role in tumor angiogenesis in ovarian cancer through regulation of miR-145 [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

The miRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1

et al. 2021

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Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low expression of miR-582-3p was noted in OC tissue and cell lines, and lower expression of miR-582-3p correlated with lower overall survival in OC patients. Knockdown of miR-582-3p promoted the proliferation and migration of OC cells, while overexpression inhibited them. TUG1, a long non-coding RNA, was found to bind to miR-582-3p, and inhibition of lncRNA TUG1 decreased viability and migration and weakened the effect of miR-582-3p knockdown in OC cells. Implantation of OC cells with reduced miR-582-3p caused increased tumor growth, while lncRNA TUG1 knockdown suppressed tumor growth and relieved the impact of reduced miR-582-3p in vivo . Phosphorylation of AKT and mTOR were significantly enhanced with decreased miR-582-3p expression, but lncRNA TUG1 knockdown attenuated this trend in vitro and in vivo . The novel miR-582-3p represses the malignant properties of OC via the AKT/mTOR signaling pathway by targeting lncRNA TUG1. This axis may represent valuable prognostic biomarkers and therapeutic targets for OC.

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Section: Introductionmentioning

confidence: 99%

The miRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1

et al. 2021

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“…To understand the interaction of the novel oxadiazoles with the PARP1 catalytic domain, the co-crystal structure of compound 33 [(9aR)-1-[(1-{2-fluoro-5-[(4-oxo-3,4-dihydrophthalazin-1-yl)methyl]benzoyl}piperidin-4-yl)carbonyl]-1,2,3,8,9,9a-hexahydro-7H-benzo[de][1,7]naphthyridin-7-one] with the PARP1 catalytic domain (PDB ID: 4HHY) was analyzed [ 41 ]. Accelrys DS version 2.5 was used for the molecular docking utilizing the previously reported protocol [ 42 , 43 ]. Compound 33 and the active oxadiazole compound 5s were docked towards the catalytic domain of PARP1.…”

Section: Resultsmentioning

confidence: 99%

Design and Activity of Novel Oxadiazole Based Compounds That Target Poly(ADP-ribose) Polymerase

et al. 2022

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Novel PARP inhibitors with selective mode-of-action have been approved for clinical use. Herein, oxadiazole based ligands that are predicted to target PARP-1 have been synthesized and screened for the loss of cell viability in mammary carcinoma cells, wherein seven compounds were observed to possess significant IC50 values in the range of 1.4 to 25 µM. Furthermore, compound 5u, inhibited the viability of MCF-7 cells with an IC50 value of 1.4µM, when compared to Olaparib (IC50 = 3.2 µM). Compound 5s also decreased cell viability in MCF-7 and MDA-MB-231 cells with IC50 values of 15.3 and 19.2 µM, respectively. Treatment of MCF-7 cells with compounds 5u and 5s produced PARP cleavage, H2AX phosphorylation and CASPASE-3 activation comparable to that observed with Olaparib. Compounds 5u and 5s also decreased foci-formation and 3D Matrigel growth of MCF-7 cells equivalent to or greater than that observed with Olaparib. Finally, in silico analysis demonstrated binding of compound 5s towardsthe catalytic site of PARP-1, indicating that these novel oxadiazoles synthesized herein may serve as exemplars for the development of new therapeutics in cancer.

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“…The standard treatment option for advanced EOC has been surgical resection followed by chemotherapy, typically platinum-based agents and paclitaxel [ 85 ]. Although this approach has led to improved survival rates, many patients experience recurrence of the disease due to the development of chemoresistance [ 86 , 87 , 88 ]. One of the reasons for chemotherapy resistance is drug-induced activation of immunosuppressive and oncogenic mechanisms in the TME, which heavily relies on a variety of chemokines [ 89 , 90 , 91 , 92 ].…”

Section: Potential Cxcl/cxcr-based Theranostic Strategiesmentioning

confidence: 99%

CXC Chemokine Signaling in Progression of Epithelial Ovarian Cancer: Theranostic Perspectives

Huang

Hao

Tan

et al. 2022

IJMS

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Patients with epithelial ovarian cancer (EOC) are often diagnosed at an advanced stage due to nonspecific symptoms and ineffective screening approaches. Although chemotherapy has been available and widely used for the treatment of advanced EOC, the overall prognosis remains dismal. As part of the intrinsic defense mechanisms against cancer development and progression, immune cells are recruited into the tumor microenvironment (TME), and this process is directed by the interactions between different chemokines and their receptors. In this review, the functional significance of CXC chemokine ligands/chemokine receptors (CXCL/CXCR) and their roles in modulating EOC progression are summarized. The status and prospects of CXCR/CXCL-based theranostic strategies in EOC management are also discussed.

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Long non-coding RNAs in recurrent ovarian cancer: Theranostic perspectives

Cited by 21 publications

References 132 publications

The miRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1

The miRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1

Design and Activity of Novel Oxadiazole Based Compounds That Target Poly(ADP-ribose) Polymerase

CXC Chemokine Signaling in Progression of Epithelial Ovarian Cancer: Theranostic Perspectives

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