MiR-148b, MiR-152/ALCAM Axis Regulates the Proliferation and Invasion of Pituitary Adenomas Cells

He, Wei; Huang, Ling; Li, Min; Yang, Yue; Chen, Zhe; Shen, Xiaoli

doi:10.1159/000485342

Cited by 25 publications

(13 citation statements)

References 49 publications

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“…Thus, they control the pathogenesis of the majority of diseases and multiple types of human cancer [2]. miRs regulate all hallmarks of cancer, including the proliferation and invasiveness [3][4][5]. According to the predominant function of given miR in a cancer cell, we can distinguish oncomiRs and tumor suppressor miRs [6].…”

Section: Introductionmentioning

confidence: 99%

Lineage-dependent role of miR-410-3p as oncomiR in gonadotroph and corticotroph pituitary adenomas or tumor suppressor miR in somatotroph adenomas via MAPK, PTEN/AKT, and STAT3 signaling pathways

et al. 2019

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Purpose miR-410-3p plays opposite roles in different cancers and may act as an oncomiR or tumor suppressor miR. The purpose of this study was to assess the role of miR-410-3p in somatotroph, gonadotroph, and corticotroph pituitary adenomas. Methods Tissue samples were obtained from 75 patients with pituitary adenoma. miR-410-3p expression was assessed using qRT-PCR performed on RNA isolated from fresh frozen samples. In vitro experiments were performed on cell lines derived from somatotroph (GH3), gonadotroph (RC-4B/C), and corticotroph (AtT-20) pituitary tumors. Cells were transfected with synthetic mimic of miR-410-3p or non-targeting scrambled-miR control. Subsequently, proliferation assays and transwell invasion assays were performed. The expression of cyclin D1, E1, and B1 in cells after transfection was determined using qRT-PCR. The activation of MAPK, PTEN/AKT and STAT3 signaling pathways were assessed using western blot. Results We have found that the level of expression of miR-410-3p differs in particular types of pituitary adenomas. miR-410-3p significantly upregulates proliferation and invasiveness of RC-4B/C and AtT-20 cells, while inhibiting GH3 cells. We observed that the levels of cyclin B1 upon transfection with miR-410-3p mimic were increased in RC-4B/C and AtT-20, yet decreased in GH3 cells. We have shown that miR-410-3p promoted the activation of MAPK, PTEN/AKT, and STAT3 signaling pathways in RC-4B/C and AtT-20 cells, but suppressed their activity in GH3 cells. Conclusions miR-410-3p acts as an oncomiR in gonadotroph and corticotroph adenoma cells, while as a tumor suppressor miR in somatotroph adenoma cells.

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Section: Introductionmentioning

confidence: 99%

Lineage-dependent role of miR-410-3p as oncomiR in gonadotroph and corticotroph pituitary adenomas or tumor suppressor miR in somatotroph adenomas via MAPK, PTEN/AKT, and STAT3 signaling pathways

et al. 2019

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“…Emerging data have demonstrated that miRNAs may act as oncogenes or tumor suppressors depending on the functions of their target genes [13]. Previous studies demonstrated that miRNAs play critical roles in pituitary tumorigenesis [14][15][16]. Deep sequencing is a technique that determines the precise order of nucleotides in a strand of DNA/ RNA.…”

mentioning

confidence: 99%

Next-generation sequencing of microRNAs reveals a unique expression pattern in different types of pituitary adenomas

Chen

et al. 2019

Endocr J

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Pituitary adenomas (PAs) are considered the most common intracranial tumor to cause serious morbidity because of dysregulated pituitary hormone secretions. Aberrant expression of microRNAs (miRNAs) is correlated with the development and function of the pituitary gland as well as the tumorigenesis of hypothalamic-pituitary axis-related pituitary tumors. In this study, we showed the differential expression patterns of miRNAs in NFPAs (nonfunctioning pituitary adenomas), GHPAs (growth hormone-secreting pituitary adenomas) and PRLPAs (prolactin-secreting pituitary adenomas) compared to those in three normal pituitary glands using the HiSeq 2000 sequencing system (Illumina). We validated miRNA expression using real-time quantitative polymerase chain reaction (RT-qPCR) analyses of samples from 73 patients (13 GHPAs, 42 NFPAs, and 18 PRLPAs) and 6 normal pituitary gland. We observed that miR-34c-3p was significantly downregulated in our PRLPA samples (p < 0.01), along with miR-34b-5p, miR-378 and miR-338-5p (all p < 0.05). In NFPAs, miR-493-5p was downregulated, and miR-181b-5p was significantly upregulated (p < 0.01). In GHPAs, miR-184 was significantly upregulated (p < 0.05). We observed that the tumor suppressive miR-124-3p was downregulated in both NFPAs and GHPAs. Taken together, we showed distinctive miRNA expression patterns in these three PAs, and these miRNA signatures in PA may have therapeutic potential as novel biomarkers for each type of PA.

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“…He et al . revealed that miR‐152/ALCAM axis modulated pituitary adenomas cells proliferation and invasion . More importantly, in lung adenocarcinama, ALCAM acted as the target of miR‐483 in regulating invasion and metastasis .…”

Section: Discussionmentioning

confidence: 97%

“… He et al . showed that inhibition expression of ALCAM repressed proliferation and invasion of pituitary adenomas cells . Moreover, Ishiguro and his colleagues revealed that knockdown of ALCAM suppressed NSCLC cell migration and invasion and that it was associated with the prognosis of NSCLC patients .…”

Section: Introductionmentioning

confidence: 98%

MiR‐148b suppressed non‐small cell lung cancer progression via inhibiting ALCAM through the NF‐κB signaling pathway

et al. 2019

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Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality worldwide. MiRNAs are recognized as important molecules in cancer biology. The aim of the study was to identify a novel biomarker miR-148b and its mechanism in the modulation of NSCLC progression. Methods: The expressional level of miR-148b was analyzed by RT-PCR. The effect of miR-4317 on proliferation was evaluated through 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2Htetrazolium bromide (MTT) assay. The effect of miR-148b on the metastasis of NSCLC was detected through transwell assays. The verification of the target of miR-148b was assessed by TargetScan and dualluciferase reporter assay. The related proteins in this study were analyzed by western blot. Results: Our findings confirmed that miR-148b was decreased in NSCLC and NSCLC patients with lower expression exhibited poorer overall survival (OS). Increasing miR-148b significantly repressed proliferation, invasion and migration. More importantly, activated leukocyte cell adhesion molecule (ALCAM) was determined as the direct target of miR-148b, and reintroduction of ALCAM attenuated miR-148b effect on the progress of NSCLC. In addition, NF-κB signaling pathway was modulated by miR-148b/ALCAM axis. Conclusions: Our results indicated that miR-148b is able to suppress NSCLC growth and metastasis via targeting ALCAM through the NF-κB pathway. These findings provided new evidence that miR-148b serves as a potential biomarker and novel target for NSCLC treatment.

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MiR-148b, MiR-152/ALCAM Axis Regulates the Proliferation and Invasion of Pituitary Adenomas Cells

Cited by 25 publications

References 49 publications

Lineage-dependent role of miR-410-3p as oncomiR in gonadotroph and corticotroph pituitary adenomas or tumor suppressor miR in somatotroph adenomas via MAPK, PTEN/AKT, and STAT3 signaling pathways

Lineage-dependent role of miR-410-3p as oncomiR in gonadotroph and corticotroph pituitary adenomas or tumor suppressor miR in somatotroph adenomas via MAPK, PTEN/AKT, and STAT3 signaling pathways

Next-generation sequencing of microRNAs reveals a unique expression pattern in different types of pituitary adenomas

MiR‐148b suppressed non‐small cell lung cancer progression via inhibiting ALCAM through the NF‐κB signaling pathway

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