scholarly journals Mitochondrial pathway mediated apoptosis and cell cycle arrest triggered by cobalt(III) complex in Dalton’s lymphoma cells

Author(s):  
Praveen Kumar Verma ◽  
Mannu Kumar Gond ◽  
Manoj Kumar Bharty ◽  
Arbind Acharya
2022 ◽  
pp. 106772
Author(s):  
Rishi Kant Singh ◽  
Praveen Kumar Verma ◽  
Sandeep Kumar ◽  
Alok Shukla ◽  
Naveen Kumar ◽  
...  

2021 ◽  
Author(s):  
Sandeep Kumar ◽  
Alok Shukla ◽  
Praveen Kumar Verma ◽  
Rishi kant Singh ◽  
Naveen Kumar ◽  
...  

Abstract Cancer is a group of diseases characterised by abnormal and undifferentiated cell growth that has the potential to spread to other parts of the body. It is the world's second leading cause of death and morbidity. According to the GLOBOCAN 2020 report, out of 19.3 million new cancer cases and 10 million deaths reported, 544352 new cases and 259793 deaths occurred by non-Hodgkin lymphoma (NHLs). Although, numerous therapeutic approaches like, surgery, radiotherapy, chemotherapy and immunotherapy have been developed to treat cancer, limited success has been achieved, possibly due to severe side effects associated with the drugs used during chemotherapy. Therefore, deciphering the novel compound with least side effects and highly potent against cancer is urgently required. In the present study we used leaf extract of M. oleifera, well-known for its anti-cancer efficacy against different cancer cells, however, its effect on Dalton’s lymphoma, a type of spontaneously occurring T cell lymphoma originated in the thymus of DBA mice is seriously lacking. Therefore, present study was aimed to analyze the therapeutic efficacy of M. oleifera against DL cells. Our results show that leaf extract of M. oleifera (MOML) significantly induces morphological changes in DL cells followed by chromatin condensation, nuclear fragmentation, and ROS generation. We also found significant changes in mitochondrial membrane potential (ΔΨm) in a dose dependent manner. Furthermore, apoptosis of DL cells induced by cell cycle arrest at G2/M and S phase suggested that MOML could be used to treat NHL effectively


Cell Cycle ◽  
2013 ◽  
Vol 12 (16) ◽  
pp. 2625-2635 ◽  
Author(s):  
Michael K Kullmann ◽  
Claudia Grubbauer ◽  
Katrin Goetsch ◽  
Heidelinde Jäkel ◽  
Silvio R Podmirseg ◽  
...  

2020 ◽  
Vol 97 ◽  
pp. 103709 ◽  
Author(s):  
Selvaraj Shyamsivappan ◽  
Raju Vivek ◽  
Arjunan Saravanan ◽  
Thangaraj Arasakumar ◽  
Thangaraj Suresh ◽  
...  

2002 ◽  
Vol 283 (2) ◽  
pp. C609-C622 ◽  
Author(s):  
Paul J. Smith ◽  
Marie Wiltshire ◽  
Sharon Davies ◽  
Suet-Feung Chin ◽  
Anthony K. Campbell ◽  
...  

Reactive changes in free intracellular zinc cation concentration ([Zn2+]i) were monitored, using the fluorescent probe Zinquin, in human lymphoma cells exposed to the DNA-damaging agent VP-16. Two-photon excitation microscopy showed that Zinquin-Zn2+ forms complexes in cytoplasmic vesicles. [Zn2+]iincreased in both p53wt (wild type) and p53mut(mutant) cells after exposure to low drug doses. In p53mutcells noncompetent for DNA damage-induced apoptosis, elevated [Zn2+]i was maintained at higher drug doses, unlike competent p53wt cells that showed a collapse of the transient before apoptosis. In p53wt cells, the [Zn2+]i rise paralleled an increase in p53 and bax-to-bcl-2 ratio but preceded an increase in p21WAF1, active cell cycle arrest in G2, or nuclear fragmentation. Reducing [Zn2+]i, using N, N, N′, N′-tetrakis(2-pyridylmethyl)ethylenediamine, caused rapid apoptosis in both p53wt and p53mut cells, although cotreatment with VP-16 exacerbated apoptosis only in p53wt cells. This may reflect changed thresholds for proapoptotic caspase-3 activation in competent cells. We conclude that the DNA damage-induced transient is p53-independent up to a damage threshold, beyond which competent cells reduce [Zn2+]i before apoptosis. Early stress responses in p53wt cells take place in an environment of enhanced Zn2+ availability.


2014 ◽  
Vol 6 ◽  
pp. 290-304 ◽  
Author(s):  
Suvitha Syam ◽  
Ahmad Bustamam ◽  
Rasedee Abdullah ◽  
Mohamed Aspollah Sukari ◽  
Najihah Mohd Hashim ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document