Analysis of anti‐apoptotic PVT1 oncogene and apoptosis‐related proteins (p53, Bcl2, PD‐1, and PD‐L1) expression in thyroid carcinoma

Ibrahiem, Afaf T.; Makhdoom, Amin K; Alanazi, Khalid S; Alanazi, Abdulaziz M.; Mukhlef, Abdulaziz M.; Elshafey, Saad H; Toraih, Eman A.; Fawzy, Manal S.

doi:10.1002/jcla.24390

Cited by 5 publications

(2 citation statements)

References 80 publications

(160 reference statements)

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“…PVT1 is located in the 8q24 region of the human chromosome, which is often amplified in the genome of cancer cells. [15][16][17][18] Thus far, most evidence indicates that PVT1 acts as an oncogene in most types of tumors, such as gastric cancer, colorectal cancer, and non-small cell lung cancer (NSCLC). [19][20][21] Furthermore, abnormal PVT1 expression has also been reported in PCa.…”

Section: Discussionmentioning

confidence: 99%

Plasmacytoma variant translocation 1 inhibits miR‐515‐5p function and modulates high mobility group B3 to promote the growth of prostate cancer cells

Zhu

Kang

et al. 2022

Andrology

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Aim:This study is performed to analyze the role of long non-coding RNA plasmacytoma variant translocation 1 in prostate cancer.Methods and materials: Plasmacytoma variant translocation 1, miR-515-5p, and high mobility group B3 mRNA expressions were examined using quantitative real-time polymerase chain reaction and immunohistochemistry. After gain-of-function and lossof-function models were established, the changes in cell proliferation, migration, and invasion were evaluated using cell counting kit-8 assay, 5-ethynyl-2′-deoxyuridine assay, and Transwell experiments. Validation of the targeting relationships between plasmacytoma variant translocation 1 and miR-515-5p, and between miR-515-5p and high mobility group B3 was conducted using bioinformatics prediction, a dualluciferase reporter assay, and an RNA immunoprecipitation experiment. Moreover, the effects of plasmacytoma variant translocation 1 and miR-515-5p on high mobility group B3 protein expression were examined using Western blot.Results: Plasmacytoma variant translocation 1 expression and high mobility group B3 expression were up-regulated in prostate cancer tissues and cell lines while miR-515-5p expression was down-regulated. Plasmacytoma variant translocation 1 knockdown restrained the proliferation, migration, and invasion of LNCaP and DU145 cells in vitro, and the transfection with miR-515-5p inhibitors reversed these effects. Mechanistically, plasmacytoma variant translocation 1 could repress the function of miR-515; high mobility group B3 was proved to be a target gene of miR-515-5p, and its expression could be indirectly positively modulated by plasmacytoma variant translocation 1. Conclusion:Plasmacytoma variant translocation 1 accelerates prostate cancer progression by repressing miR-515-5p's function to upregulate high mobility group B3 expression.

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Section: Discussionmentioning

confidence: 99%

Plasmacytoma variant translocation 1 inhibits miR‐515‐5p function and modulates high mobility group B3 to promote the growth of prostate cancer cells

Zhu

Kang

et al. 2022

Andrology

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“…(1) c-Myc-Targeting PVT1 and Cell Functions PVT1 modulating cell functions are summarized in Table 5. PVT1 inhibits apoptosis of colon [171] and thyroid [172] cancer cells. PVT1 promotes the autophagy of liver cancer cells [173].…”

Section: Akt Effector (C-myc)-targeting Lncrnas and Cell Functionsmentioning

confidence: 99%

Long Noncoding RNAs and Circular RNAs Regulate AKT and Its Effectors to Control Cell Functions of Cancer Cells

Tang

Chuang

Shiau

et al. 2022

Cells

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AKT serine-threonine kinase (AKT) and its effectors are essential for maintaining cell proliferation, apoptosis, autophagy, endoplasmic reticulum (ER) stress, mitochondrial morphogenesis (fission/fusion), ferroptosis, necroptosis, DNA damage response (damage and repair), senescence, and migration of cancer cells. Several lncRNAs and circRNAs also regulate the expression of these functions by numerous pathways. However, the impact on cell functions by lncRNAs and circRNAs regulating AKT and its effectors is poorly understood. This review provides comprehensive information about the relationship of lncRNAs and circRNAs with AKT on the cell functions of cancer cells. the roles of several lncRNAs and circRNAs acting on AKT effectors, such as FOXO, mTORC1/2, S6K1/2, 4EBP1, SREBP, and HIF are explored. To further validate the relationship between AKT, AKT effectors, lncRNAs, and circRNAs, more predicted AKT- and AKT effector-targeting lncRNAs and circRNAs were retrieved from the LncTarD and circBase databases. Consistently, using an in-depth literature survey, these AKT- and AKT effector-targeting database lncRNAs and circRNAs were related to cell functions. Therefore, some lncRNAs and circRNAs can regulate several cell functions through modulating AKT and AKT effectors. This review provides insights into a comprehensive network of AKT and AKT effectors connecting to lncRNAs and circRNAs in the regulation of cancer cell functions.

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