Long noncoding RNA PANDA promotes esophageal squamous carcinoma cell progress by dissociating from NF-YA but interact with SAFA

Sep 10, 2019Pathology, research and practice

Long noncoding RNA PANDA helps esophageal cancer cells grow by separating from one protein (NF-YA) but binding to another (SAFA)

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Abstract

PANDA expression was up-regulated in cancerous tissues from 134 patients and 9 ESCC cell lines.

Higher PANDA levels in ESCC tissues are associated with advanced clinical stage and shorter overall survival.
Down-regulation of PANDA significantly suppresses ESCC cell proliferation and colony formation by halting the G1-S checkpoint transition.
Depletion of PANDA leads to reduced levels of E2F1, cyclin D1, cyclin D2, cyclin E1, and Bcl-2.
PANDA interacts with NF-YA and SAFA, influencing the expression of genes related to cell proliferation and apoptosis.
PANDA may serve as a potential prognostic biomarker and therapeutic target for esophageal squamous cell carcinoma.

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Esophageal squamous cell carcinoma (ESCC) is one of the major global health problems, especially in Asia. Long non-coding RNAs (lncRNAs) have been increasingly identified and characterized in almost every aspect of biology, especially in cancer biology. This research desires to explore the regulatory mechanism of lncRNA PANDA (PANDA) on ESCC process. Quantitative real-time PCR (qRT-PCR) was carried out to detect the PANDA expression, which was up-regulated in matched cancerous tissues and adjacent noncancerous tissues from 134 patients and 9 ESCC cell lines. Higher expression of PANDA in ESCC tissues was associated with TNM stage, advanced clinical stage, and shorter overall survival of ESCC patients by MTT, EDU, colony formation assay and ﬂow cytometry in KYSE180 and KYSE450 cells. Exogenous down-regulation of PANDA expression signiﬁcantly suppressed ESCC cells proliferation and colony formation by arresting G1-S checkpoint transition in vitro, and retarded the development of tumors in vivo. Meanwhile, qRT-PCR and western blot assays showed that depletion of PANDA reduced E2F1, cyclinD1, cyclinD2, cyclinE1 and Bcl-2 expression. RIP showed the interaction between PANDA and NF-YA or SAFA. Our findings suggested that, PANDA drifted away from NF-YA to promote the expression of NF-YA-E2F1 co-regulated proliferation-promoting genes, and to limit the cell apoptosis. In addition, PANDA binds SAFA to switch on the tumor proliferation program through CyclinD1/2-Cyclin E1 and Bcl-2 pathways. PANDA could serve as a potential prognostic biomarker and therapeutic target for ESCC.

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Long noncoding RNA PANDA promotes esophageal squamous carcinoma cell progress by dissociating from NF-YA but interact with SAFA

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