Common tools for pituitary adenomas research: cell lines and primary cells

Zhu, Ziyan; Cui, Weiwei; Zhu, Danyan; Gao, Nailin; Zhu, Yiping

doi:10.1007/s11102-019-01003-4

Cited by 14 publications

(9 citation statements)

References 70 publications

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“…Immortalized cell lines and primary cells are indispensable tools in the study of cancer pathogenesis and have been shown to share similar pathophysiological changes [ 37 ]. However, some studies have found that there are some differences between cell lines and primary cells in their protein properties, morphology, and metabolic activity [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-106b-5p regulates esophageal squamous cell carcinoma progression by binding to HPGD

et al. 2022

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Background Several studies have documented the key role of microRNAs (miRNAs) in esophageal squamous cell carcinoma (ESCC). Although the expression of the 15-hydroxyprostaglandin dehydrogenase (HPGD) gene and miR-106b-5p are reportedly linked to cancer progression, their underlying mechanisms in ESCC remain unclear. Methods mRNA and miRNA expression in ESCC tissues and cells were analyzed using RT-qPCR. Luciferase and RNA pull-down assays were used to identify the interaction between miR-106b-5p and HPGD. Xenograft and pulmonary metastasis models were used to assess tumor growth and metastasis. CCK-8, BrdU, colony formation, adhesion, cell wound healing, Transwell, and caspase-3/7 activity assays, and flow cytometry and western blot analyses were used to examine the function of miR-106-5p and HPGD in ESCC cell lines. Results The findings revealed that miR-106b-5p expression was upregulated in ESCC tissues and cell lines. miR-106b-5p augmented cellular proliferation, colony formation, adhesion, migration, invasion, and proportion of cells in the S-phase, but reduced apoptosis and the proportion of cells in G1-phase. Silencing of miR-106-5p inhibited tumor growth in vivo and pulmonary metastasis. Although HPGD overexpression suppressed proliferation, colony formation, adhesion, migration, and invasion of ESCC cells, it promoted apoptosis and caused cell cycle arrest of the ESCC cells. The results also indicated a direct interaction of HPGD with miR-106b-5p in ESCC cells. Furthermore, miR-106b-5p inhibited HPGD expression, thereby suppressing ESCC tumorigenesis. Conclusion Our data suggest that miR-106b-5p enhances proliferation, colony formation, adhesion, migration, and invasion, and induces the cycle progression, but represses apoptosis of ESCC cells by targeting HPGD. This suggests that the miR-106b-5p/HPGD axis may serve as a promising target for the diagnosis and treatment of ESCC.

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Section: Discussionmentioning

confidence: 99%

MiR-106b-5p regulates esophageal squamous cell carcinoma progression by binding to HPGD

et al. 2022

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“…First, the sample sizes of previous PA studies were small and should be further expanded. Second, it is also difficult to immortalize primary cells from PAs and to maintain stable passage and hormone expression ( 85 ). Finally, few research teams exist worldwide, and funding is limited.…”

Section: Discussionmentioning

confidence: 99%

Tumor-Associated Macrophages: New Horizons for Pituitary Adenoma Researches

Han

Lin

et al. 2021

Front. Endocrinol.

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Macrophages are one of the most common infiltrating immune cells and an essential component of tumor microenvironment. Macrophages and the soluble cytokines and chemokines produced play an important role in tumorigenesis, progression, invasion and metastasis in solid tumors. Despite the multiple studies in other solid tumors, there is little known about macrophages in pituitary adenomas. Recently, studies about pituitary adenoma-infiltrated macrophages have been emerging, including the immunohistochemical and immunophenotypic analysis of the pituitary adenomas and further studies into the mechanism of the crosstalk between macrophages and tumor cells in vivo and in vitro. These studies have offered us new insights into the polarization of macrophages and its role in tumorigenesis, progression and invasion of pituitary adenomas. This review describes the advances in the field of pituitary adenoma-infiltrated macrophages and the prospect of targeting macrophages as cancer therapy in pituitary adenoma.

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“…GH3 was cultured in DMEM medium (Gibco, 12430047) supplemented with 10% fetal bovine serum (FBS; Gibco, 10270-106), and MMQ was cultured in RPMI-1640 medium (Gibco, 31800105) supplemented with 10% FBS (BI, 1928702), in an incubator with 5% CO 2 at 37°C. MMQ cells secrete prolactin and GH3 cells secrete both growth hormone and prolactin, and they are appropriate cell models used in the study of prolactima (37).…”

Section: Cell Culturementioning

confidence: 99%

PBK/TOPK Inhibitor Suppresses the Progression of Prolactinomas

et al. 2022

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BackgroundProlactinoma is the most common type of pituitary tumors, and its resultant tumor occupying and hormone disturbance greatly damage the health of patients. In this study, we investigated a protein kinase-PDZ Binding Kinase (PBK)/T-LAK Cell-Originated Protein Kinase (TOPK) as a candidate protein regulating prolactin (PRL) secretion and tumor growth of prolactinomas.MethodsDownloaded prolactinoma transcriptome dataset from Gene Expression Omnibus (GEO) database, and screened differentially expressed genes (DEGs) between normal pituitary tissues and prolactinoma tissues. Then, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of DEGs were performed, a protein-protein interaction (PPI) network was constructed and the hub genes were identified. After a literature search, TOPK was presumed as an candidate target regulating the prolactinoma. We found a specific inhibitor of TOPK to investigate its effects on the proliferation, migration, apoptosis and PRL secretion of pituitary tumor cells. Finally, the regulation of TOPK inhibitor on its downstream target-p38 Mitogen Activated Protein Kinase (p38 MAPK) was detected to explore the potential mechanism.ResultsA total of 361 DEGs were identified, and 20 hub genes were screened out. TOPK inhibitor HI-TOPK-032 could suppress the proliferation & migration and induce apoptosis of pituitary tumor cells in vitro, and reduce PRL secretion and tumor growth in vivo. HI-TOPK-032 also inhibited the phosphorylation level of the downstream target p38 MAPK, suggesting that TOPK inhibitors regulate the development of prolactinoma by mediating p38 MAPK.ConclusionOur study of identification and functional validation of TOPK suggests that this candidate can be a promising molecular target for prolactinoma treatment.

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Common tools for pituitary adenomas research: cell lines and primary cells

Cited by 14 publications

References 70 publications

MiR-106b-5p regulates esophageal squamous cell carcinoma progression by binding to HPGD

MiR-106b-5p regulates esophageal squamous cell carcinoma progression by binding to HPGD

Tumor-Associated Macrophages: New Horizons for Pituitary Adenoma Researches

PBK/TOPK Inhibitor Suppresses the Progression of Prolactinomas

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