β4GalT-II increases cisplatin-induced apoptosis in HeLa cells depending on its Golgi localization

2007 ◽  
Vol 358 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Jianhai Jiang ◽  
Jin Zhou ◽  
Yuanyan Wei ◽  
Jialin Shen ◽  
Dan Liu ◽  
...  
Keyword(s):  
Hela Cells ◽  
Golgi Localization ◽  
Induced Apoptosis

scholarly journals Depletion of Survivin suppresses docetaxel-induced apoptosis in HeLa cells by facilitating mitotic slippage

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Teng-Long Han ◽  
Hang Sha ◽  
Jun Ji ◽  
Yun-Tian Li ◽  
Deng-Shan Wu ◽  
...  
Keyword(s):  
Hela Cells ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Clonogenic Survival ◽  
Mitotic Arrest ◽  
Apoptosis Pathway ◽  
Mitotic Slippage ◽  
Intrinsic Apoptosis Pathway ◽  
Apoptosis Protein ◽  
Induced Apoptosis

AbstractThe anticancer effects of taxanes are attributed to the induction of mitotic arrest through activation of the spindle assembly checkpoint. Cell death following extended mitotic arrest is mediated by the intrinsic apoptosis pathway. Accordingly, factors that influence the robustness of mitotic arrest or disrupt the apoptotic machinery confer drug resistance. Survivin is an inhibitor of apoptosis protein. Its overexpression is associated with chemoresistance, and its targeting leads to drug sensitization. However, Survivin also acts specifically in the spindle assembly checkpoint response to taxanes. Hence, the failure of Survivin-depleted cells to arrest in mitosis may lead to taxane resistance. Here we show that Survivin depletion protects HeLa cells against docetaxel-induced apoptosis by facilitating mitotic slippage. However, Survivin depletion does not promote clonogenic survival of tumor cells but increases the level of cellular senescence induced by docetaxel. Moreover, lentiviral overexpression of Survivin does not provide protection against docetaxel or cisplatin treatment, in contrast to the anti-apoptotic Bcl-xL or Bcl-2. Our findings suggest that targeting Survivin may influence the cell response to docetaxel by driving the cells through aberrant mitotic progression, rather than directly sensitizing cells to apoptosis.

Bid and Calpains Cooperate to Trigger Oxaliplatin-Induced Apoptosis of Cervical Carcinoma HeLa Cells

2009 ◽  
Vol 76 (5) ◽  
pp. 998-1010 ◽  
Author(s):  
Sergio Anguissola ◽  
Barbara Köhler ◽  
Robert O'Byrne ◽  
Heiko Düssmann ◽  
Mary D. Cannon ◽  
...  
Keyword(s):  
Cervical Carcinoma ◽  
Hela Cells ◽  
Induced Apoptosis

Triazole/thiadiazole substituted 4'-demethylepipodophyllotoxin derivatives induced apoptosis in HeLa cells by up-regulating TMEM133

2021 ◽  
pp. 174189
Author(s):  
Wei Zhao ◽  
Ying Duan ◽  
Hong-Mei Li ◽  
Shengying Li ◽  
Yuemao Shen ◽  
...  
Keyword(s):  
Hela Cells ◽  
Induced Apoptosis

scholarly journals Lysosome Dysfunction Enhances Oxidative Stress-Induced Apoptosis through Ubiquitinated Protein Accumulation in Hela Cells

2012 ◽  
Vol 296 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Chunyan Yu ◽  
Xiaowei Huang ◽  
Ye Xu ◽  
Hongyan LI ◽  
Jing Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hela Cells ◽  
Protein Accumulation ◽  
Ubiquitinated Protein ◽  
Induced Apoptosis

scholarly journals SPATA4 Counteracts Etoposide-Induced Apoptosis via Modulating Bcl-2 Family Proteins in HeLa Cells

2015 ◽  
Vol 38 (10) ◽  
pp. 1458-1463 ◽  
Author(s):  
Junjun Jiang ◽  
Liyuan Li ◽  
Mingchao Xie ◽  
Ryosuke Fuji ◽  
Shangfeng Liu ◽  
...  
Keyword(s):  
Hela Cells ◽  
Induced Apoptosis

scholarly journals Shiga toxin signals via ATP and its effect is blocked by purinergic receptor antagonism

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Karl E. Johansson ◽  
Anne-Lie Ståhl ◽  
Ida Arvidsson ◽  
Sebastian Loos ◽  
Ashmita Tontanahal ◽  
...  
Keyword(s):  
Hela Cells ◽  
Shiga Toxin ◽  
Calcium Influx ◽  
Purinergic Receptor ◽  
Atp Release ◽  
Retrograde Transport ◽  
P2x Receptor ◽  
P2x1 Receptor ◽  
Uremic Syndrome ◽  
Induced Apoptosis

Abstract Shiga toxin (Stx) is the main virulence factor of enterohemorrhagic Escherichia coli (EHEC), that cause gastrointestinal infection leading to hemolytic uremic syndrome. The aim of this study was to investigate if Stx signals via ATP and if blockade of purinergic receptors could be protective. Stx induced ATP release from HeLa cells and in a mouse model. Toxin induced rapid calcium influx into HeLa cells, as well as platelets, and a P2X1 receptor antagonist, NF449, abolished this effect. Likewise, the P2X antagonist suramin blocked calcium influx in Hela cells. NF449 did not affect toxin intracellular retrograde transport, however, cells pre-treated with NF449 exhibited significantly higher viability after exposure to Stx for 24 hours, compared to untreated cells. NF449 protected HeLa cells from protein synthesis inhibition and from Stx-induced apoptosis, assayed by caspase 3/7 activity. The latter effect was confirmed by P2X1 receptor silencing. Stx induced the release of toxin-positive HeLa cell- and platelet-derived microvesicles, detected by flow cytometry, an effect significantly reduced by NF449 or suramin. Suramin decreased microvesicle levels in mice injected with Stx or inoculated with Stx-producing EHEC. Taken together, we describe a novel mechanism of Stx-mediated cellular injury associated with ATP signaling and inhibited by P2X receptor blockade.

Potentiation of etoposide-induced apoptosis in HeLa cells by co-treatment with KG-135, a quality-controlled standardized ginsenoside formulation

2010 ◽  
Vol 294 (1) ◽  
pp. 74-81 ◽  
Author(s):  
Won-Hee Lee ◽  
Joon-Seok Choi ◽  
Hyun Young Kim ◽  
Jeong-Hill Park ◽  
Byoung Duck Park ◽  
...  
Keyword(s):  
Hela Cells ◽  
Induced Apoptosis

ATF5 increases cisplatin-induced apoptosis through up-regulation of Cyclin D3 transcription in HeLa cells

2006 ◽  
Vol 339 (2) ◽  
pp. 591-596 ◽  
Author(s):  
Yuanyan Wei ◽  
Jianhai Jiang ◽  
Maoyun Sun ◽  
Xiaoning Chen ◽  
Hanzhou Wang ◽  
...  
Keyword(s):  
Hela Cells ◽  
Cyclin D3 ◽  
Induced Apoptosis
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