scholarly journals Typhonium flagelliforme decreases telomerase expression in HeLa cervical cancer cells

Author(s):  
Endang Purwaningsih ◽  
Yulia Suciati ◽  
Etty Widayanti

<p><strong>Background</strong><br /> Cancer cells have a relatively high telomerase activity compared to normal cells, so that cancer cells have the ability for continued proliferation and uncontrolled mitosis. Telomerase is an enzyme responsible for the length of telomeres, DNA segments located at the ends of eukaryotic chromosomes. Natural materials such as rodent tuber (<em>Typhonium flagelliforme</em>) have anticancer potential. The purpose of the present study was to determine the effects of <em>Typhonium flagelliforme </em>extract on telomerase expression in HeLa cervical cancer and T47D breast cancer cells.</p><p><br /> <strong>Methods </strong></p><p>This experimental laboratory study was conducted on cultured HeLa and T47D cancer cell lines, with normal Vero cells as controls, and using RPMI and M199 culture media. The study comprised three groups, i.e. controls, and groups receiving <em>Typhonium flagelliforme </em>extract at doses of ½ IC50 and IC50. Telomerase expression was measured by immunohistochemistry (IHC). Analysis of variance and LSD multiple comparison test were used to analyze the data.</p><p><strong> </strong></p><p><strong>Results </strong><br /> Telomerase expression in cancer cells showed significantly higher values compared to normal Vero cells. <em>Typhonium flagelliforme</em> extract was capable of significantly decreasing telomerase expression in cancer cells receiving the extract.</p><p><strong> </strong></p><strong>Conclusion </strong><br /> <em>Typhonium flagelliforme</em> extract at different doses is capable of decreasing telomerase expression more effectively in cervical cancer cells than in breast cancer cells. This study shows that <em>Typhonium flagelliforme</em> may have anti-cancer activity, necessitating further investigations.

2021 ◽  
Vol 19 (02) ◽  
pp. 99-109
Author(s):  
HASMAH ABDULLAH ◽  
NORLIDA MAMAT ◽  
NOR MUNIRAH ZAKARIA ◽  
NUR IMAN FATIHAH MOHD YUNAN ◽  
MUHAMMAD IRFAN NOOR HISHAM ◽  
...  

2017 ◽  
Vol 268 ◽  
pp. 254-258 ◽  
Author(s):  
Nur Shafawati Rosli ◽  
Azhar Abdul Rahman ◽  
Azlan Abdul Aziz ◽  
Shaharum Shamsuddin ◽  
Nurul Sabihah Zakaria

Ultrastructural characteristic and morphological changes of untreated and treated breast cancer MCF-7 cells were observed by energy-filtered transmission electron microscope (EFTEM). Morphological observation of MCF-7 after being treated with 13 nm, 50 nm, and 70 nm AuNPs, were looking unhealthy and dying out of the populace, the observed cells were more reduced and dying as treatment with 50 nm and 70 nm AuNPs. Cells detachment, clumping, shrunken, and dispersed cells in the culture medium and floating cells were also observed. The observed morphological changes increase in 50 nm and 70 nm AuNPs than in 13 nm AuNPs, which is less toxic to MCF-7 cells. The presented morphological analysis has established that 13 nm AuNPs showed less toxic to MCF-7 breast cancer cells. Whereas, control cells of MCF-7 were treated with only complete culture media, despite the duration of treatment, whereby the cells maintained most of their morphological features and observed to have a typical morphology of healthy cells that are well attached to the surface. These results indicate that AuNPs were clustered in the cells and there was no significant difference between images of different sizes of AuNPs observed in the cells, because the AuNPs always clustered together inside the cells.


2006 ◽  
Vol 291 (1) ◽  
pp. C40-C49 ◽  
Author(s):  
Ken-ichi Kiyomiya ◽  
Ming-Shyue Lee ◽  
I-Chu Tseng ◽  
Hong Zuo ◽  
Robert J. Barndt ◽  
...  

Matriptase and its cognate inhibitor, hepatocyte growth factor activator inhibitor-1 (HAI-1), have been implicated in carcinoma onset and malignant progression. However, the pathological mechanisms of matriptase activation are not defined. Steroid sex hormones play crucial roles in prostate and breast cancer. Therefore, we investigated the questions of whether and how steroid sex hormones regulate matriptase activation in these cancer cells. Treatment of cells with 17β-estradiol had no effect on activation of matriptase in hormone-starved breast cancer cells, in part due to their high constitutive level of activated matriptase. In striking contrast, very low levels of activated matriptase were detected in hormone-starved lymph node prostatic adenocarcinoma (LNCaP) cells. Robust activation of matriptase was observed as early as 6 h after exposure of these cells to 5α-dihydrotestosterone (DHT). Activation of matriptase was closely followed by shedding of the activated matriptase with >90% of total activated matriptase present in the culture media 24 h after DHT treatment. Activated matriptase was shed in a complex with HAI-1 and may result from simultaneously proteolytic cleavages of both membrane-bound proteins. Latent matriptase and free HAI-1 were also shed into culture media. As a result of shedding, the cellular levels of matriptase and HAI-1 were significantly reduced 24 h after exposure to DHT. DHT-induced matriptase activation and shedding were significantly inhibited by the androgen antagonist bicalutamide, by the RNA transcription inhibitor actinomycin D, and by the protein synthesis inhibitor cycloheximide. These results suggest that in LNCaP cells, androgen induces matriptase activation via the androgen receptor, and requires transcription and protein synthesis.


2001 ◽  
Vol 33 (3) ◽  
pp. 156-163 ◽  
Author(s):  
Yong Wook Kim ◽  
Soo Young Hur ◽  
Tae Eung Kim ◽  
Joon Mo Lee ◽  
Sung Eun Namkoong ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 867
Author(s):  
Aleksandra Romaniuk-Drapała ◽  
Ewa Totoń ◽  
Natalia Konieczna ◽  
Marta Machnik ◽  
Wojciech Barczak ◽  
...  

Telomerase is known to contribute to telomere maintenance and to provide cancer cell immortality. However, numerous reports are showing that the function of the enzyme goes far beyond chromosome ends. The study aimed to explore how telomerase downregulation in MCF7 and MDA-MB-231 breast cancer cells affects their ability to survive. Consequently, sensitivity to drug resistance, proliferation, and adhesion were assessed. The lentiviral-mediated human telomerase reverse transcriptase (hTERT) downregulation efficiency was performed at gene expression and protein level using qPCR and Western blot, respectively. Telomerase activity was evaluated using the Telomeric Repeat Amplification Protocol (TRAP) assay. The study revealed that hTERT downregulation led to an increased sensitivity of breast cancer cells to doxorubicin which was demonstrated in MTT and clonogenic assays. During a long-term doubling time assessment, a decreased population doubling level was observed. Interestingly, it did not dramatically affect cell cycle distribution. hTERT downregulation was accompanied by an alteration in β1-integrin- and by focal adhesion kinase (FAK)-driven pathways together with the reduction of target proteins phosphorylation, i.e., paxillin and c-Src. Additionally, autophagy activation was observed in MDA-MB-231 cells manifested by alternations in Atg5, Beclin 1, LC3II/I ratio, and p62. These results provide new evidence supporting the possible therapeutic potential of telomerase downregulation leading to induction of autophagy and cancer cells elimination.


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