RETRACTED ARTICLE: Long noncoding RNA HAGLROS promotes the process of mantle cell lymphoma by regulating miR-100/ATG5 axis and involving in PI3K/AKT/mTOR signal

Abstract

This research planned to grab the expression and impact of lncRNA HAGLROS in the biology and progression of mantle cell lymphoma. HAGLROS level in mantle cell lymphoma cell lines was detected, followed by investigation of the influences of HAGLROS silencing on Mino cell biological performances. Afterwards, the express patterns of HAGLROS vs. miR-100, as well as miR-100 vs. ATG5, were investigated. Furthermore, whether HAGLROS could regulate the signals of PI3K/AKT/mTOR was analyzed. HAGLROS level was high in mantle cell lymphoma cell lines. Silencing of HAGLROS inhibited Mino cell viability, increased apoptosis and decreased autophagy by sponging miR-100. Moreover, miR-100 targeted ATG5 fixed. Furthermore, HAGLROS suppression resulted in inhibition on the briskness of PI3K/ AKT/mTOR signals. Concurrently HAGLROS suppression and miR-100 inhibitor markedly changed the impacts of HAGLROS down-regulation alone on activating PI3K/AKT/mTOR signals, which could further change after co-transfection of si-HAGLROS þ miR-100 inhibitor þ siATG5. Our findings point out that expression of HAGLROS is increased in mantle cell lymphoma cells and may function as an oncogene in mantle cell lymphoma. HAGLROS may promote tumour development by regulating miR-100/ATG5/ PI3K/AKT/mTOR axis.

[Retracted] Circular RNA circCCDC66 Contributes to Malignant Phenotype of Osteosarcoma by Sponging miR‐338‐3p to Upregulate the Expression of PTP1B

“…Recently, with the rapid development of biology, more and more RNA biomolecules are used as clinical markers of cancer [24]. For example, microRNA-195, microRNA-223, microRNA-221, microRNA-421, and microRNA-203 in serum are differently expressed in OS tissues, indicating that they can be used as a new biomarker for screening OS to predict poor prognosis and monitor the progress of cancer [17,[25][26][27][28]. In the present study, we found that circCCDC66 was overexpressed in tumor cells compared to normal tissues.…”

Protective properties of heme oxygenase-1 expressed in umbilical cord mesenchymal stem cells help restore the ovarian function of premature ovarian failure mice through activating the JNK/Bcl-2 signal pathway-regulated autophagy and upregulating the circulating of CD8+CD28− T cells

“…Meanwhile, in mice transplanted with HO-1-MSCs or treated with anisomycin, the autophagy in GCs can be obviously activated, shown as increased levels of LC3-II, beclin1, and Atg5 but decreased p62. It is known that increased levels of autophagosomes can enhance its own formation and/or block the lysosomal processing [45]. In this study, decreased number of autophagosomes and receded intensity of fluorescence by MDC were observed in mice transplanted with shHO-1-MSCs or treated with SP600125, also with the observation of nucleolus shrinked and chromatin condensation.…”

ZEB1-AS1/miR-133a-3p/LPAR3/EGFR axis promotes the progression of thyroid cancer by regulating PI3K/AKT/mTOR pathway

“…PI3K/AKT/mTOR pathway is commonly accepted as a vital pathway in controlling cancer progression, and lncRNA as ceRNA has been validated to mediate tumorigenesis and development through PI3K/AKT/ mTOR pathway [24,25]. LPAR3 has been manifested to be tightly related to PI3K/AKT pathway in ovarian cancer [16].…”

“…Due to the significance of PI3K/AKT/mTOR pathway as well as its close relation to lncRNA-mediated ceRNA mechanism [24,25], we wondered whether ZEB1-AS1 involved in this pathway. Through western blot assay, the protein levels of PI3K, AKT and mTOR were hardly changed, whereas their phosphorylation levels were remarkably weakened in ZEB1-AS1 silenced cells, and partially rescued by LPAR3 overexpression.…”