Pseudogene AKR1B10P1 enhances tumorigenicity and regulates epithelial‐mesenchymal transition in hepatocellular carcinoma via stabilizing SOX4

Hao, Fang; Fei, Xiaochun; Ren, Xinping; Xiao, Joanna Xi; Chen, Yongjun; Wang, Junqing

doi:10.1111/jcmm.15790

Cited by 18 publications

(16 citation statements)

References 41 publications

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“…In hepatocellular carcinoma (HCC), higher PDIA3P1 level is associated with poorer recurrence-free survival [59]. A group of pseudogenes, AKR1B10P1, DUXAP8, MSTO2P, PDPK2P, SUMO1P3, RACGAP1P, ANXA2P2, AURKAPS1, PTTG3P, and POU5F1B, is upregulated in HCC patient tissues and cell lines [60][61][62][63][64][65][66][67][68][69]. Higher expression of DUXAP8 is associated with shorter OS and RFS time.…”

Section: Cancers Located In the Abdomen And Bonesmentioning

confidence: 99%

“…GOLGA2P10 is upregulated in HCC tissues and cells treated with ER stress inducers (tunicamycin and thapsigargin) [74]. AKR1B10P was found to be overexpressed in patient metastatic tissues and cell lines [60,61]. PDIA3P1 is upregulated in multiple cancer types and following treatment with DNA-damaging chemotherapeutic agents such as doxorubicin (Dox) [59].…”

Section: Cancers Located In the Abdomen And Bonesmentioning

confidence: 99%

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The World of Pseudogenes: New Diagnostic and Therapeutic Targets in Cancers or Still Mystery Molecules?

Stasiak

Kolenda

Kozłowska-Masłoń

et al. 2021

Life

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Pseudogenes were once considered as “junk DNA”, due to loss of their functions as a result of the accumulation of mutations, such as frameshift and presence of premature stop-codons and relocation of genes to inactive heterochromatin regions of the genome. Pseudogenes are divided into two large groups, processed and unprocessed, according to their primary structure and origin. Only 10% of all pseudogenes are transcribed into RNAs and participate in the regulation of parental gene expression at both transcriptional and translational levels through senseRNA (sRNA) and antisense RNA (asRNA). In this review, about 150 pseudogenes in the different types of cancers were analyzed. Part of these pseudogenes seem to be useful in molecular diagnostics and can be detected in various types of biological material including tissue as well as biological fluids (liquid biopsy) using different detection methods. The number of pseudogenes, as well as their function in the human genome, is still unknown. However, thanks to the development of various technologies and bioinformatic tools, it was revealed so far that pseudogenes are involved in the development and progression of certain diseases, especially in cancer.

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Section: Cancers Located In the Abdomen And Bonesmentioning

confidence: 99%

Section: Cancers Located In the Abdomen And Bonesmentioning

confidence: 99%

The World of Pseudogenes: New Diagnostic and Therapeutic Targets in Cancers or Still Mystery Molecules?

Stasiak

Kolenda

Kozłowska-Masłoń

et al. 2021

Life

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“…For instance, silenced SOX2 gene expression could reduce the growth rate of HCC xenografts and enhance the therapeutic response in HCC [ 41 , 42 ]. SOX4 was reported to modulate the endothelial cell migration and angiogenesis in HCC, and it could act as a biomarker in hepatitis B virus-associated HCC [ 43 – 46 ]. SOX8 was significantly upregulated in HCC and its upregulation promoted cancer cell proliferation in HCC [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

The Dysregulation of SOX Family Correlates with DNA Methylation and Immune Microenvironment Characteristics to Predict Prognosis in Hepatocellular Carcinoma

et al. 2022

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Background. Due to the molecular heterogeneity of hepatocellular carcinoma (HCC), majority of patients respond poorly among various of therapy. This study is aimed at conducting a comprehensive analysis about roles of SOX family in HCC for obtaining more therapeutic targets and biomarkers which may bring new ideas for the treatment of HCC. Methods. UALCAN, Kaplan Meier plotter, cBioPortal, STRING, WebGestalt, Metascape, TIMER 2.0, DiseaseMeth, MethSurv, HPA, CCLE database, and Cytoscape software were used to comprehensively analyze the bioinformatic data. Results. SOX2, SOX4, SOX8, SOX10, SOX11, SOX12, SOX17, and SOX18 were significantly differentially expressed in HCC and normal tissues and were valuable for the grade and survival of HCC patients. In addition, the gene alterations of SOX family happened frequently, and SOX4 and SOX17 had the highest mutation rate. The function of SOX family on HCC may be closely correlated with the regulation of angiogenesis-related signaling pathways. Moreover, SOX4, SOX8, SOX11, SOX12, SOX17, and SOX18 were correlation with 8 types of immune cells (including CD8+ T cell, CD4+ T cell, B cell, Tregs, neutrophil, macrophage, myeloid DC, and NK cell), and we found that most types of immune cells had a positive correlation with SOX family. Notably, CD4+ T cell and macrophage were positively related with all these SOX family. NK cells were negatively related with most SOX family genes. DNA methylation levels in promoter area of SOX2, SOX4, and SOX10 were lower in HCC than normal tissues, while SOX8, SOX11, SOX17, and SOX18 had higher DNA methylation levels than normal tissues. Moreover, higher DNA methylation level of SOX12 and SOX18 demonstrated worse survival rates in patients with HCC. Conclusion. SOX family genes could predict the prognosis of HCC. In addition, the regulation of angiogenesis-related signaling pathways may participate in the development of HCC. DNA methylation level and immune microenvironment characteristics (especially CD4+ T cell and macrophage immune cell infiltration) could be a novel insight for predicting prognosis in HCC.

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“…It also participates in the process of EMT. Whether AKR1B10 plays a specific function in GC associated with the EMT process is poorly understood [ 33 , 34 ]. In this paper, we explored whether inhibition of AKR1B10 could affect proliferation and migration of GC cells, which may depend on the EMT process.…”

Section: Discussionmentioning

confidence: 99%

AKR1B10 inhibits the proliferation and migration of gastric cancer via regulating epithelial-mesenchymal transition

Shao

Wu²,

et al. 2021

Aging

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Gastric cancer (GC) is a common malignancy around the world with a poor prognosis. Aldo-keto reductase family 1 member B10 (AKR1B10) is indispensable to cancer development and progression, which has served as a diagnostic biomarker for tumors. In our study, we demonstrated that the expression of AKR1B10 in GC tissues was significantly lower compared with normal gastric tissues. Subgroup analysis showed that, according to the clinic-pathological factors, the effect of the AKR1B10 expression level on the prognosis of GC patients was significantly different. Moreover, reduced expression of AKR1B10 promoted the ability of GC cells in proliferation and migration. Furthermore, increased AKR1B10 levels resulted in the opposite trend in vitro . Moreover, AKR1B10 was correlated with epithelial-mesenchymal transition (EMT) in a significant way. In vivo experiment, knockdown of AKR1B10 promoted the growth of tumor, increased Vimentin, and E-cadherin significantly. In summary, AKR1B10 is considered as a tumor suppressor in GC and is a promising therapeutic target.

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Pseudogene AKR1B10P1 enhances tumorigenicity and regulates epithelial‐mesenchymal transition in hepatocellular carcinoma via stabilizing SOX4

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 18 publications

References 41 publications

The World of Pseudogenes: New Diagnostic and Therapeutic Targets in Cancers or Still Mystery Molecules?

The World of Pseudogenes: New Diagnostic and Therapeutic Targets in Cancers or Still Mystery Molecules?

The Dysregulation of SOX Family Correlates with DNA Methylation and Immune Microenvironment Characteristics to Predict Prognosis in Hepatocellular Carcinoma

AKR1B10 inhibits the proliferation and migration of gastric cancer via regulating epithelial-mesenchymal transition

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