Mechanism of long-chain non-coding RNA hypoxia-inducible factor 1α-antisense RNA 1 regulating chemotherapy resistance of retinoblastoma by inhibiting hypoxia-inducible factor-α expression

2021 ◽  
Vol 11 (11) ◽  
pp. 1874-1880
Author(s):  
Cao Gu ◽  
Qing Li ◽  
Shaofei Zhao ◽  
Yu Gao ◽  
Peirong Lu
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Cell Survival ◽  
Treatment Effectiveness ◽  
Hypoxia Inducible Factor ◽  
Chemotherapy Resistance ◽  
Non Coding Rna ◽  
Reduce Cell Proliferation ◽  
Factor Α ◽  
Infants And Young Children

Retinoblastoma (Rb) mostly occurs in infants and young children with weak resistance. Surgical treatment causes great damage to children’s appearance, so adjuvant chemotherapy is needed to reduce the damage. But chemotherapeutic resistance affects treatment effectiveness and may even lead to the death of the child. Exploring the specific mechanism of drug resistance in Rb children is helpful to improve the therapeutic effect. It was found that the relative expression in Rb cell Y79, SO-Rb50, and HXO-Rb44 was greatly higher than that in normal hum an retinal cells. After transfection of SI-HIF1A-AS1 into Rb cells, the expression of lncRNA HIF1A-AS1 was decreased greatly, and the level of HIF-1α was down-regulated. Suppress lncRNA HIF1A-AS1 expression can reduce cell proliferation and improve apoptosis. Based on the overexpression of HIF-1α, the cell proliferation ability was restored partially, and the apoptosis ability was reduced greatly. When cells were cultured with vincristine, we found that suppress lncRNA HIF1A-AS1 expression can decrease cell survival, and overexpression of HIF-1α improved cell survival. The above results confirmed that inhibition of lncRNA HIF1AAS1 expression could reduce drug resistance of Y97 cells, while overexpression of HIF-1α can antagonize the drug resistance of low expression lncRNA HIF1A-AS1 against Rb cells. Therefore, this study suggests that lncRNA HIF1A-AS1 may regulate Rb cells’ resistance to vincristine by regulating HIF-1α expression.

Research Progress of Axl Inhibitors

2019 ◽  
Vol 19 (15) ◽  
pp. 1338-1349 ◽  
Author(s):  
Zhi-Gang Sun ◽  
Jian-Hua Liu ◽  
Jin-Mai Zhang ◽  
Yong Qian
Keyword(s):  
Skeletal Muscle ◽  
Signal Transduction ◽  
Cell Proliferation ◽  
Drug Resistance ◽  
Receptor Tyrosine Kinase ◽  
Chemotherapy Resistance ◽  
Research Progress ◽  
Invasion And Metastasis ◽  
Over Expression ◽  
Pancreatic Cancers

Axl, a Receptor Tyrosine Kinase (RTK) belonging to the TAM (Axl, Mer, Tyro3) family, participates in many signal transduction cascades after mostly being stimulated by Growth arrestspecific 6(Gas6). Axl is widely expressed in many organs, such as macrophages, endothelial cells, heart, liver and skeletal muscle. Over-expression and activation of Axl are associated with promoting chemotherapy resistance, cell proliferation, invasion and metastasis in many human cancers, such as breast, lung, and pancreatic cancers. Therefore, the research and development of Axl inhibitors is of great significance to strengthen the means of cancer treatment, especially to solve the problem of drug resistance. Axl inhibitors have attracted more and more researchers' attention in recent years. This review discusses the research progress of Axl inhibitors in recent years.

scholarly journals Long Non-coding RNA EPIC1 Promotes Cell Proliferation and Motility and Drug Resistance in Glioma

2020 ◽  
Vol 17 ◽  
pp. 130-137
Author(s):  
Jianjiao Wang ◽  
Shuguang Yang ◽  
Qiongyu Ji ◽  
Qingsong Li ◽  
Fenggang Zhou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Non Coding Rna ◽  
Long Non Coding Rna

The regulation, localization, and functions of oxygen-sensing prolyl hydroxylase PHD3

2013 ◽  
Vol 394 (4) ◽  
pp. 449-457 ◽  
Author(s):  
Panu M. Jaakkola ◽  
Krista Rantanen
Keyword(s):  
Cell Survival ◽  
Hypoxia Inducible Factor ◽  
Oxygen Sensors ◽  
Cell Type ◽  
Low Oxygen ◽  
Von Hippel Lindau ◽  
Low Oxygen Tension ◽  
Cellular Oxygen ◽  
Domain Protein ◽  
Factor Α

Abstract The prolyl 4-hydroxylase domain protein 3 (PHD3) belongs to 2-oxoglutarate and iron-dependent dioxygenases. Together with the two closest paralogues, PHD1 and PHD2, these enzymes have been identified as cellular oxygen sensors that can mark the hypoxia-inducible factor α (HIF-α) for von Hippel-Lindau protein-mediated proteasomal destruction. Although having overlapping functions with PHD1 and PHD2, PHD3 markedly differs from the two isoforms. PHD3 shows a different expression pattern and subcellular localization as well as activity under low oxygen tension. Moreover, it has the widest range of non-HIF targets underlying its diverse functions. The functions of PHD3 differ depending on the cell type and also partially on the microenvironmental conditions it is expressed at. Under normoxia, PHD3 has been shown to be proapoptotic, but under hypoxia, it can have cell survival or proliferation-supporting functions. Here we discuss the regulation, targets, and functions of PHD3.

scholarly journals Tight Control of Hypoxia-inducible Factor-α Transient Dynamics Is Essential for Cell Survival in Hypoxia

2014 ◽  
Vol 289 (9) ◽  
pp. 5549-5564 ◽  
Author(s):  
James Bagnall ◽  
Joseph Leedale ◽  
Sarah E. Taylor ◽  
David G. Spiller ◽  
Michael R. H. White ◽  
...  
Keyword(s):  
Cell Survival ◽  
Hypoxia Inducible Factor ◽  
Transient Dynamics ◽  
Tight Control ◽  
Factor Α

scholarly journals Inhibition of Kelch-like epichlorohydrin-related protein 1 promotes the progression and drug resistance of lung adenocarcinoma

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11908
Author(s):  
Hong Gao ◽  
Peipei Tang ◽  
Kejie Ni ◽  
Lun Zhu ◽  
Song Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Drug Resistance ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Lung Adenocarcinoma ◽  
Chemotherapy Resistance ◽  
Related Protein ◽  
H1299 Cell ◽  
Node Metastasis

Background Lung cancer is a common malignant carcinoma of respiratory system with high morbidity and mortality. Kelch-like epichlorohydrin-related protein 1 (Keap1), a member of the BTB-Kelch protein family, has been reported as an important molecule in several cancers. However, its potential role in tumor is still controversial. Here we aim to clarify the effect of Keap1 on the biological characteristics and chemotherapy resistance in lung adenocarcinoma (LUAD). Methods Immunohistochemistry was conducted to compare Keap1 expression in lung adenocarcinoma tissues and matched non-cancerous tissues, and the correlation between Keap1 expression and clinicopathological features was analyzed. Subsequently, the stable A549 and H1299 cell lines with Keap1 knockdown or overexpression were constructed using lentivirus. The roles of Keap1 on the cell proliferation, migration, invasion and drug resistance were investigated by colony formation assay, cell proliferation assay, wound scratch test, transwell invasion assay and drug sensitivity assay, respectively. Results Keap1 was lowly expressed in tumor tissues compared to matched non-cancerous tissues, and its expression was correlated with TNM stage and lymph node metastasis. Early stage (I) tumors without lymph node metastasis had higher levels of Keap1 expression compared with late-stage tumors (II, III) with the presence of lymphatic metastasis. Colony formation assays showed that Keap1 knockdown promoted the proliferation of A549 and H1299 cells, and the cell growth curves further confirmed this feature. In contrast, wound scratch and transwell invasion experiments showed that Keap1 overexpression inhibited cell migration and invasive malignancy. The IC50 for cisplatin and paclitaxel were significantly increased by Keap1 knockdown in A549 and H1299 cell lines. Conclusion Keap1 knockdown promotes tumor cell growth, proliferation, invasion, metastasis and chemotherapy resistance in LUAD. It may be a potential tumor marker to guide the staging and treatment of lung cancer.

scholarly journals Long non‐coding RNA POU6F2‐AS2 promotes cell proliferation and drug resistance in colon cancer by regulating miR‐377/BRD4

2020 ◽  
Vol 24 (7) ◽  
pp. 4136-4149
Author(s):  
Guangru Xu ◽  
Hongxing Zhu ◽  
Jinhua Xu ◽  
Yan Wang ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Drug Resistance ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Glutathione S-Transferases in Cancer

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 701
Author(s):  
Rahul Raj Singh ◽  
Katie M. Reindl
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Clinical Trials ◽  
Antioxidant Enzymes ◽  
Cancer Treatment ◽  
Cell Survival ◽  
Structural Similarity ◽  
Cancer Development ◽  
Pharmacological Studies ◽  
Glutathione S Transferases

In humans, the glutathione S-transferases (GST) protein family is composed of seven members that present remarkable structural similarity and some degree of overlapping functionalities. GST proteins are crucial antioxidant enzymes that regulate stress-induced signaling pathways. Interestingly, overactive GST proteins are a frequent feature of many human cancers. Recent evidence has revealed that the biology of most GST proteins is complex and multifaceted and that these proteins actively participate in tumorigenic processes such as cell survival, cell proliferation, and drug resistance. Structural and pharmacological studies have identified various GST inhibitors, and these molecules have progressed to clinical trials for the treatment of cancer and other diseases. In this review, we discuss recent findings in GST protein biology and their roles in cancer development, their contribution in chemoresistance, and the development of GST inhibitors for cancer treatment.

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