Ras-Mediated Activation of NF-κB and DNA Damage Response in Carcinogenesis

Ahmad, Anas; Ahsan, Haseeb

doi:10.1080/07357907.2020.1721523

Cited by 19 publications

(10 citation statements)

References 193 publications

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“…One of the key causative factors in severity of cancer cases and pathophysiology process is oxidative stress. A moderate increase in ROS level often induces cell proliferation, whereas excessive amounts of ROS induce cell cycle arrest and finally apoptosis [ 55 ]. The mechanism of apoptosis induction in COLON-26 cells by Ba-SeNp-Mo was determined by measuring the intracellular ROS level by measuring the oxidation of nonfluorescent DCFH-DA to its highly fluorescent derivative DCF.…”

Section: Resultsmentioning

confidence: 99%

Pharmacological Prospects of Morin Conjugated Selenium Nanoparticles—Evaluation of Antimicrobial, Antioxidant, Thrombolytic, and Anticancer Activities

Nirmala,

Sridevi,

Aishwarya

et al. 2023

BioNanoSci.

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Selenium nanoparticles (SeNPs) have gained wide importance in the scientific community and have emerged as an optimistic therapeutic carrier agent for targeted drug delivery. In the present study, the effectiveness of nano selenium conjugated with Morin (Ba-SeNp-Mo) produced from endophytic bacteria Bacillus endophyticus reported in our earlier research was tested against various Gram-positive, Gram-negative bacterial pathogens and fungal pathogens that showed good zone of inhibition against all selected pathogens. Antioxidant activities of these NPs were studied by 1, 1-diphenyl-2- picrylhydrazyl (DPPH), 2,2′-Azino-bis-3-ethylbenzothiozoline-6-sulfonic acid (ABTS), hydrogen peroxide (H 2 O 2 ), superoxide (O 2 − ), and nitric oxide (NO) radical scavenging assays that exhibited dose-dependent free radical scavenging activity with IC 50 values 6.92 ± 1.0, 16.85 ± 1.39, 31.60 ± 1.36, 18.87 ± 1.46, and 6.95 ± 1.27 μg/mL. The efficiency of DNA cleavage and thrombolytic activity of Ba-SeNp-Mo were also studied. The antiproliferative effect of Ba-SeNp-Mo was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in COLON-26 cell lines that resulted in IC 50 value of 63.11 μg/mL. Further increased intracellular reactive oxygen species (ROS) levels up to 2.03 and significant early, late and necrotic cells were also observed in AO/EtBr assay. CASPASE 3 expression was upregulated to 1.22 (40 μg/mL) and 1.85 (80 μg/mL) fold. Thus, the current investigation suggested that the Ba-SeNp-Mo has offered remarkable pharmacological activity. Graphical Abstract

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Section: Resultsmentioning

confidence: 99%

Pharmacological Prospects of Morin Conjugated Selenium Nanoparticles—Evaluation of Antimicrobial, Antioxidant, Thrombolytic, and Anticancer Activities

Nirmala,

Sridevi,

Aishwarya

et al. 2023

BioNanoSci.

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“…EBV latency involves the expression of EBV latency-associated genes 4 , which often result in the dysregulation of the cell cycle, causing unregulated progression of the G1/S phase and inhibition of apoptosis 87 . Checkpoint kinase 2 ( CHEK-2 ) is a tumor suppressor gene that encodes for serine-threonine kinase (CHK2) and is involved in the regulation of apoptosis, cell cycle arrest, and DNA repair 88 . We found a 1.6-fold higher expression of CHEK-2 in EBV-positive PCa tissues compared to EBV-negative PCa samples, indicating that the presence of EBV in the tissue might be associated with the dysregulation of CHEK-2 gene expression.…”

Section: Discussionmentioning

confidence: 99%

Differential analysis of histopathological and genetic markers of cancer aggressiveness, and survival difference in EBV-positive and EBV-negative prostate carcinoma

Ahmed,

Sheikh,

Fatima

et al. 2024

Sci Rep

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Several studies have shown an association between prostate carcinoma (PCa) and Epstein-Barr virus (EBV); however, none of the studies so far have identified the histopathological and genetic markers of cancer aggressiveness associated with EBV in PCa tissues. In this study, we used previously characterized EBV-PCR-positive (n = 39) and EBV-negative (n = 60) PCa tissues to perform an IHC-based assessment of key histopathological and molecular markers of PCa aggressiveness (EMT markers, AR expression, perineural invasion, and lymphocytic infiltration characterization). Additionally, we investigated the differential expression of key oncogenes, EMT-associated genes, and PCa-specific oncomiRs, in EBV-positive and -negative tissues, using the qPCR array. Finally, survival benefit analysis was also performed in EBV-positive and EBV-negative PCa patients. The EBV-positive PCa exhibited a higher percentage (80%) of perineural invasion (PNI) compared to EBV-negative PCa (67.3%) samples. Similarly, a higher lymphocytic infiltration was observed in EBV-LMP1-positive PCa samples. The subset characterization of T and B cell lymphocytic infiltration showed a trend of higher intratumoral and tumor stromal lymphocytic infiltration in EBV-negative tissues compared with EBV-positive tissues. The logistic regression analysis showed that EBV-positive status was associated with decreased odds (OR = 0.07; p-value < 0.019) of CD3 intratumoral lymphocytic infiltration in PCa tissues. The analysis of IHC-based expression patterns of EMT markers showed comparable expression of all EMT markers, except vimentin, which showed higher expression in EBV-positive PCa tissues compared to EBV-negative PCa tissues. Furthermore, gene expression analysis showed a statistically significant difference (p < 0.05) in the expression of CDH1, AR, CHEK-2, CDKN-1B, and CDC-20 and oncomiRs miR-126, miR-152-3p, miR-452, miR-145-3p, miR-196a, miR-183-3p, and miR-146b in EBV-positive PCa tissues compared to EBV-negative PCa tissues. Overall, the survival proportion was comparable in both groups. The presence of EBV in the PCa tissues results in an increased expression of certain oncogenes, oncomiRs, and EMT marker (vimentin) and a decrease in CD3 ITL, which may be associated with the aggressive forms of PCa.

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“…[ 19 , 20 ] Tumors are fundamentally caused by DNA damage to genetic material. [ 21 , 22 , 23 ] Abnormalities in the DNA damage repair pathway promote genomic instability during Cd exposure, and ultimately drive the malignant transformation of lung epithelial cells. Interestingly, DNA damage has been shown to be accompanied by abnormal expression of non‐coding circRNAs.…”

Section: Discussionmentioning

confidence: 99%

circCIMT Silencing Promotes Cadmium‐Induced Malignant Transformation of Lung Epithelial Cells Through the DNA Base Excision Repair Pathway

Chen

Cui

et al. 2023

Advanced Science

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Changes in gene expression in lung epithelial cells are detected in cancer tissues during exposure to pollutants, highlighting the importance of gene‐environmental interactions in disease. Here, a Cd‐induced malignant transformation model in mouse lungs and bronchial epithelial cell lines is constructed, and differences in the expression of non‐coding circRNAs are analyzed. The migratory and invasive abilities of Cd‐transformed cells are suppressed by circCIMT. A significant DNA damage response is observed after exposure to Cd, which increased further following circCIMT‐interference. It is found that APEX1 is significantly down‐regulated following Cd exposure. Furthermore, it is demonstrated that circCIMT bound to APEX1 during Cd exposure to mediate the DNA base excision repair (BER) pathway, thereby reducing DNA damage. In addition, simultaneous knockdown of both circCIMT and APEX1 promotes the expression of cancer‐related genes and malignant transformation after long‐term Cd exposure. Overall, these findings emphasis the importance of genetic‐epigenetic interactions in chemical‐induced cancer transformation.

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Ras-Mediated Activation of NF-κB and DNA Damage Response in Carcinogenesis

Cited by 19 publications

References 193 publications

Pharmacological Prospects of Morin Conjugated Selenium Nanoparticles—Evaluation of Antimicrobial, Antioxidant, Thrombolytic, and Anticancer Activities

Pharmacological Prospects of Morin Conjugated Selenium Nanoparticles—Evaluation of Antimicrobial, Antioxidant, Thrombolytic, and Anticancer Activities

Differential analysis of histopathological and genetic markers of cancer aggressiveness, and survival difference in EBV-positive and EBV-negative prostate carcinoma

circCIMT Silencing Promotes Cadmium‐Induced Malignant Transformation of Lung Epithelial Cells Through the DNA Base Excision Repair Pathway

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