Tumor suppressor protein p53 exerts negative transcriptional regulation on human sodium iodide symporter gene expression in breast cancer

Kelkar, Madhura; Thakur, Bhushan; Derle, Abhishek; Chatterjee, Sushmita; Ray, Pritha; De, Abhijit

doi:10.1007/s10549-017-4297-2

Cited by 21 publications

(21 citation statements)

References 52 publications

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“…An image analysis software (Image-Proplus) was employed at high magnification (Media Cybernetics, Silver Spring, MD, USA) in order to determine the average OD value involving positive staining of LFA-1, MMP-9, and Caspase-3 in the hippocampal CA1 area of rat brain tissues respectively, with a quantitative analysis performed soon after. Cells with brownish-yellow appearance were considered protein-positive ones [10]. The judgment criteria of positive protein levels were as follows: five high-power fields of vision for each section were randomly selected (× 200), with 100 cells selected for each field; the percentage was then calculated using the formula: percentage of positive cells = positive tumor cells/total tumor cells × 100% (> 10% as positive [+]; < 10% as negative [-]).…”

Section: Terminal Deoxynucleotidyl Transferase (Tdt)-mediated (Dutp) mentioning

confidence: 99%

Lentivirus-Mediated Gene Silencing of Lymphocyte Function-Associated Antigen 1 Inhibits Apoptosis of Hippocampal Neurons in Rats with Acute Cerebral Ischemia After Cerebral Lymphatic Blockage

Yu¹,

Li²,

Che³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Cerebral ischemia is considered to be the most common cause of stroke with high mortality. It occurs as a result of the damage of the hippocampal neurons with lymphocyte function–associated antigen (LFA)-1 being emphasized to play a role in the biological functions of hippocampal neurons. This study was conducted in order to investigate the effects of specific knockdown of LFA-1 expression by lentivirus had on the apoptosis of the hippocampal neurons, simulated by rat models of acute cerebral ischemia after cerebral lymphatic blockage. Methods: A total of 60 Wistar rats were selected as subjects, among which 50 were used to establish models of the acute cerebral ischemia after cerebral lymphatic blockage, while the remaining 10 rats were treated with the sham operation. The underlying regulatory mechanisms regarding LFA-1 were analyzed with the treatment of si-LFA-1 and LFA-1 vector in the hippocampal CA1 area of brain tissues isolated from the rats with acute cerebral ischemia. The brain water content, electrolyte content, and blood-brain barrier permeability located in ischemic area of rats were measured. TUNEL staining and immunochemistry methods were employed in order to determine the apoptosis rate and positive levels of LFA-1, MMP-9, and Caspase-3. The mRNA and protein levels of related genes were also detected by means of RT-qPCR and western blot assay. Results: The brain water content, Na⁺ and Ca⁺ contents, blood-brain barrier permeability, apoptosis rate, positive levels of LFA-1, MMP-9, and Caspase-3 were decreased, and the K⁺ content was increased in ischemic tissues treated with si-LFA-1. The mRNA and protein levels of LFA-1, MMP-9, Caspase-3, and Bax had all decreased, while the mRNA and protein levels of Bcl-2 were elevated in the hippocampal CA1 area of rat brain tissues treated with si-LFA-1. These situations could be reversed through the up-regulation of LFA-1. Conclusion: In conclusion, LFA-1 gene silencing could improve the acute cerebral ischemia after cerebral lymphatic blockage by inhibiting apoptosis of the hippocampal neurons in rats.

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Section: Terminal Deoxynucleotidyl Transferase (Tdt)-mediated (Dutp) mentioning

confidence: 99%

Lentivirus-Mediated Gene Silencing of Lymphocyte Function-Associated Antigen 1 Inhibits Apoptosis of Hippocampal Neurons in Rats with Acute Cerebral Ischemia After Cerebral Lymphatic Blockage

Yu¹,

Li²,

Che³

et al. 2018

Cell Physiol Biochem

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“…After three PBS washes, diaminobenzidine (DAB) (Beijing Bioss, Beijing, China) was employed for tissue colouration at room temperature, after which the sections were immersed in haematoxylin for 5 minutes, washed with running water, rinsed in 1% hydrochloric ethanol for 4 seconds and treated under running water for 20 minutes to visualize a blue colour. The Image‐Proplus image analysis software (Media Cybernetics, Silver Springs, MD) was employed to determine the average optical density (OD) value of HOXC8 positive staining, with brown‐yellow coloured cells observed at high magnification. Five fields of vision (×400) were randomly selected from each section with 200 cells from each field, with the percentage of positive cells calculated accordingly.…”

Section: Methodsmentioning

confidence: 99%

Down‐regulation of long non‐coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up‐regulation of microRNA‐204

Wang

Tan²,

Zhuang³

et al. 2019

J Cellular Molecular Medi

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Oesophageal cancer is a progressive tumour with high mortality. However, therapies aimed at treating oesophageal cancer remain relatively limited. Accumulating studies have highlighted long non‐coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR), microRNA‐204 (miR‐204) and homeobox C8 (HOXC8) in the progression of oesophageal cancer. Herein, we tried to demonstrate the function of HOTAIR, miR‐204 and HOXC8 in oesophageal cancer and their relationship. Differentially expressed genes involved in oesophageal cancer were identified. The endogenous expression of HOTAIR and miR‐204 in oesophageal cancer cell lines was altered to elucidate their effects and to identify the interaction among HOTAIR, miR‐204 and HOXC8. We also explored the underlying regulatory mechanisms of HOTAIR and miR‐204 with siRNA against HOTAIR, miR‐204 mimic or miR‐204 inhibitor. Cell proliferation, migration, invasion and apoptosis were subsequently detected. Xenograft in nude mice was induced to evaluate tumourigenicity. miR‐204 was down‐regulated, while HOTAIR and HOXC8 were up‐regulated in the oesophageal cancer tissues. HOTAIR could competitively bind to miR‐204 and miR‐204 could further target HOXC8. The oesophageal cancer cells treated with si‐HOTAIR or miR‐204 mimic exhibited decreased expression levels of HOXC8, Vimentin and MMP‐9, but increased E‐cadherin level. Silenced HOTAIR or elevated miR‐204 inhibited proliferation, migration and invasion, along with stimulated apoptosis of oesophageal cancer cells. In summary, our results show that lncRNA HOTAIR could specifically bind to miR‐204 as a competing endogenous RNA and regulate miR‐204 and HOXC8. Hence, down‐regulation of HOTAIR could inhibit progression of oesophageal cancer, indicating a novel target for oesophageal cancer treatment.

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“…21 The criterion for judging positive protein expression was as follows: each section was randomly selected with five high magnification field, 100 cells in per field were counted, and the positive cells were rated according to its percentage. Afterward, the sections were supplemented with 100 μL 5% bovine serum albumin, 100 μL primary antibody THBS1 (1:200; ab93653; Abcam Inc., Cambridge, MA) and biotin-labeled goat anti-rabbit secondary antibody working solution (1:100; HY90046; Hengyuan Biological Technology Co Ltd, Shanghai, China), and streptomycin anti biotin peroxidase solution (Zhongshan Biotechnology Co, Beijing, China).…”

Section: Immunohistochemistrymentioning

confidence: 99%

MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

Yang

Liu

2019

J of Cellular Biochemistry

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Chronic idiopathic urticaria (CIU) is a polyetiological dermatologic disease. Reports have stated that some microRNAs (miRNAs) have their roles to play in inflammatory response. In this present study, we aim to investigate whether miR‐194 has an effect on attenuating inflammatory response and human dermal microvascular endothelial cells (HDMECs) permeability of CIU mast cells through TGF‐β/SMAD pathway by binding to thrombospondin 1 (THBS1). The Gene Expression Omnibus database was used to obtain the CIU‐related microarray data, and then the analysis of differentially expressed genes was conducted and the miRNA regulated by THBS1 was predicted. After transfection of different mimic, inhibitor, or small interfering RNA, the effect of miR‐194 on inflammatory reaction, mast cell degranulation, histamine release rate, HDMECs permeability, and the expression of THBS1, interferon γ (IFN‐γ), TGF‐β, Smad3, and interleukin 4 (IL‐4) were detected. THBS1 was verified to be the miR‐194 target. After transfected with overexpressed miR‐194 and si‐THBS1, the degranulation rate, histamine release rate, and HDMECs permeability were significantly reduced, while the expression of IFN‐γ was higher, and the expression of THBS1, TGF‐β, Smad3, IL‐4 was significantly lower, accompanied with alleviated inflammatory reaction. Our study provides evidence that miR‐194 negatively modulates THBS1 and inhibits the activation of TGF‐β/SMAD pathway, thereby alleviating the inflammatory response and HDMECs permeability of mast cells in CIU.

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Tumor suppressor protein p53 exerts negative transcriptional regulation on human sodium iodide symporter gene expression in breast cancer

Cited by 21 publications

References 52 publications

Lentivirus-Mediated Gene Silencing of Lymphocyte Function-Associated Antigen 1 Inhibits Apoptosis of Hippocampal Neurons in Rats with Acute Cerebral Ischemia After Cerebral Lymphatic Blockage

Lentivirus-Mediated Gene Silencing of Lymphocyte Function-Associated Antigen 1 Inhibits Apoptosis of Hippocampal Neurons in Rats with Acute Cerebral Ischemia After Cerebral Lymphatic Blockage

Down‐regulation of long non‐coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up‐regulation of microRNA‐204

MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

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