Effect of lncRNA HULC knockdown on rat secreting pituitary adenoma GH3 cells

Rui, Qiu Hong; Bo, Jun; Liao, Yu; Dai, Jin; Zhang, Cai

doi:10.1590/1414-431x20197728

Cited by 7 publications

(6 citation statements)

References 39 publications

(47 reference statements)

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“…Overexpression of a subgroup of long noncoding RNAs, termed “highly up-regulated in liver cancer” (HULC), promoted GH3 cell viability, migration, invasion, and PRL and GH secretion with knockdown inducing apoptosis ( 286 ).…”

Section: Epigenetic Mechanisms Of Tumorigenesismentioning

confidence: 99%

Novel Insights into Pituitary Tumorigenesis: Genetic and Epigenetic Mechanisms

Nadhamuni

Korbonits

2020

Endocrine Reviews

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Substantial advances have been made recently in the pathobiology of pituitary tumors. Similar to many other endocrine tumors, over the last few years we have recognized the role of germline and somatic mutations in a number of syndromic or non-syndromic conditions with pituitary tumor predisposition. These include the identification of novel germline variants in patients with familial or simplex pituitary tumors and establishment of novel somatic variants identified through next generation sequencing. Advanced techniques have allowed the exploration of epigenetic mechanisms mediated through DNA methylation, histone modifications and non-coding RNAs, such as microRNA, long noncoding RNAs and circular RNAs. These mechanisms can influence tumor formation, growth and invasion. While genetic and epigenetic mechanisms often disrupt similar pathways, such as cell cycle regulation, in pituitary tumors there is little overlap between genes altered by germline, somatic and epigenetic mechanisms. The interplay between these complex mechanisms driving tumorigenesis are best studied in the emerging multi-omics studies. Here, we summarize insights from the recent developments in the regulation of pituitary tumorigenesis.

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Section: Epigenetic Mechanisms Of Tumorigenesismentioning

confidence: 99%

Novel Insights into Pituitary Tumorigenesis: Genetic and Epigenetic Mechanisms

Nadhamuni

Korbonits

2020

Endocrine Reviews

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“…Therefore, it is important to clarify which factors affect the secretory mechanism of GH. Many studies have reported that miRNAs can affect GH secretion [ 35 , 56 , 57 ]. However, research on circRNAs that regulate GH secretion, especially circRNAs that act as molecular sponges of miRNAs, is rare.…”

Section: Discussionmentioning

confidence: 99%

CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells

Ren

Zhang

et al. 2021

Animals

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CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT–PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT–PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT–PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.

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“…HULC suppresses Beclin-1 phosphorylation, thus reducing autophagy, via the mTOR pathway (19). Knockdown of HULC inhibits pituitary adenoma GH3 cells via the up-regulation of miR-130b, the down-regulation of Forkhead box M1 (FOXM1), and the activation of the phosphoinositide-3kinase/serine-threonine kinase Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) and Janus kinase-1 (JAK1)/ signal transducer and activator of transcription-3 (STAT3) pathways (20). These results demonstrated that HULC knockdown inhibited HepG2 cells proliferation and invasion abilities in vitro, as well as tumor growth in vivo, and promoted the survival of the mice.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HULC shRNA disinhibits miR-377-5p to suppress the growth and invasion of hepatocellular carcinoma in vitro and hepatocarcinogenesis in vivo

Cao¹,

Wei²,

Han³

et al. 2020

Ann Transl Med

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Background: Aberrant expression of up-regulated long non-coding RNA [LncRNA highly upregulated in liver cancer (HULC)] has been observed to play an important regulatory role in the development of multiple human diseases. However, the molecular mechanism underlying the role of HULC and miR-377-5p in HCC needs to be urgently explored. Methods:The mRNA and protein expression levels of HULC were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot in hepatocellular carcinoma (HCC) cell line HB611, HepG2 and H22, respectively. HULC-shRNA was transfected into HepG-2 cells, which were randomly divided into the control, shRNA-NC, and sh-HULC groups. The correlation between HULC and miR-377-5p was analyzed by performing a luciferase reporter assay. The targeting relationship between miR-377-5p and hypoxia-inhibitory factor-1α (HIF-1α) was also investigated using a luciferase reporter assay.Sh-HULC and miR-377-5p inhibitors were transfected either alone or together into HepG2 cells, and which were divided into the control group, the sh-HULC group, the miR-377-5p inhibitor, and the sh-HULC + inhibitor group for subsequent experiments. HepG2 cell proliferation and invasion were measured by 5-Ethynyl-2-Deoxyuridine (EdU) staining and Transwell invasion assay, respectively. Western plot was carried out to detect the protein expression levels of Ki67, PCNA, E-cadherin, and N-cadherin.Tumor xenograft mouse models were established to confirm the effect of HULC down-regulation on the development of HCC in vivo.Results: The mRNA and protein expression levels of HULC were markedly increased, whereas the mRNA expression levels of miR-377-5p were decreased in HCC cell lines. HepG2 cell proliferation and invasion were suppressed in the Sh-HULC group, while miR-377-5p showed the opposite. Further experiments exhibited that miR-377-5p was targeted by HULC, and an negative correlation between HULC and miR-377-5p was observed. Importantly, the in vivo experiments indicated that down-regulation of HULC could inhibit tumor growth. Taken together, our research demonstrated that down-regulation of HULC plays an anti-cancer role through restrainingHepG2 cell proliferation and invasion.Conclusions: In summary, our in vitro and in vivo findings confirmed HULC to play a role in the progression of HCC, with the underlying mechanism possibly involving the miR-377-5p/HIF-1α pathway.

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Effect of lncRNA HULC knockdown on rat secreting pituitary adenoma GH3 cells

Cited by 7 publications

References 39 publications

Novel Insights into Pituitary Tumorigenesis: Genetic and Epigenetic Mechanisms

Novel Insights into Pituitary Tumorigenesis: Genetic and Epigenetic Mechanisms

CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells

LncRNA HULC shRNA disinhibits miR-377-5p to suppress the growth and invasion of hepatocellular carcinoma in vitro and hepatocarcinogenesis in vivo

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