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Apoptosis and Cell Signaling in Disease
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Apoptosis and Cell Signaling in Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 8131

Special Issue Editor

Dr. Jean-Pierre Jaffrézou

E-Mail Website
Guest Editor
CNRS UMR5549, CerCo, TMBI, CHU Purpan, Pavillon Baudot, 31059 Toulouse, France
Interests: cancer therapies; chemoresistance; microdomains; cell signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Apoptosis is an active process of genetically controlled self-destruction, which controls cell homeostasis, tissue morphogenesis or the development and functioning of the immune system. The regulation of apoptosis at several levels is essential to maintain the delicate balance between cellular survival and death signalling that is required to prevent disease. Despite important theoretical advances, little progress has been made in the treatment or prevention of diseases associated with the disruption of cell death (such as cancers, neurodegenerative and autoimmune syndromes or viral infections). This Special Issue will discuss the recent advances in the field, thereby contributing to our knowledge on how the selective inclusion or exclusion of key signalling pathways play a role in signal transduction, apoptosis, disease and many other cellular events.

Dr. Jean-Pierre Jaffrézou
Guest Editor

Manuscript Submission Information

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Keywords

  • apoptosis
  • cell signaling
  • disease
  • cancer
  • cellular senescence
  • cellular damage
  • therapy resistance

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Published Papers (4 papers)

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Research

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18 pages, 7475 KiB  
Article
Isolinderalactone Induces Apoptosis, Autophagy, Cell Cycle Arrest and MAPK Activation through ROS–Mediated Signaling in Colorectal Cancer Cell Lines
by Jith-Shyan Chen, Sheng-Chun Chiu, Sung-Ying Huang, Shu-Fang Chang and Kuan-Fu Liao
Int. J. Mol. Sci. 2023, 24(18), 14246; https://doi.org/10.3390/ijms241814246 - 18 Sep 2023
Cited by 6 | Viewed by 1775
Abstract
Colorectal cancer (CRC) is one of the most common malignancies worldwide. Isolinderalactone (ILL), a sesquiterpene isolated from the root extract of Lindera aggregata, has been reported to exhibit anti–proliferative and anti–metastatic activities in various cancer cell lines. However, the mechanisms associated with [...] Read more.
Colorectal cancer (CRC) is one of the most common malignancies worldwide. Isolinderalactone (ILL), a sesquiterpene isolated from the root extract of Lindera aggregata, has been reported to exhibit anti–proliferative and anti–metastatic activities in various cancer cell lines. However, the mechanisms associated with its antitumor effects on CRC cells remain unclear. ILL treatment significantly suppressed proliferation and induced cell cycle G2/M arrest in CRC cells by inhibiting the expression of cyclin B, p–cdc2, and p–cdc25c and up–regulating the expression of p21. In addition, ILL induced mitochondria–associated apoptosis through the up–regulation of cleaved –caspase–9 and –3 expression. ILL induced autophagy by increasing the levels of LC3B in CRC cells, which was partially rescued by treatment with an autophagy inhibitor (chloroquine). Furthermore, ILL increases the accumulation of reactive oxygen species (ROS) and activates the MAPK pathway. Application of the ROS scavenger, N–acetyl cysteine (NAC), effectively inhibited ILL toxicity and reversed ILL–induced apoptosis, cell cycle arrest, autophagy, and ERK activation. Taken together, these results suggest that ILL induces G2/M phase arrest, apoptosis, and autophagy and activates the MAPK pathway via ROS–mediated signaling in human CRC cells. Full article
(This article belongs to the Special Issue Apoptosis and Cell Signaling in Disease)
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17 pages, 3914 KiB  
Article
UPR-Induced miR-616 Inhibits Human Breast Cancer Cell Growth and Migration by Targeting c-MYC
by Vahid Arabkari, Afrin Sultana, David Barua, Mark Webber, Terry Smith, Ananya Gupta and Sanjeev Gupta
Int. J. Mol. Sci. 2023, 24(17), 13034; https://doi.org/10.3390/ijms241713034 - 22 Aug 2023
Cited by 3 | Viewed by 1828
Abstract
C/EBP homologous protein (CHOP), also known as growth arrest and DNA damage-inducible protein 153 (GADD153), belongs to the CCAAT/enhancer-binding protein (C/EBP) family. CHOP expression is induced by unfolded protein response (UPR), and sustained CHOP activation acts as a pivotal trigger for ER stress-induced [...] Read more.
C/EBP homologous protein (CHOP), also known as growth arrest and DNA damage-inducible protein 153 (GADD153), belongs to the CCAAT/enhancer-binding protein (C/EBP) family. CHOP expression is induced by unfolded protein response (UPR), and sustained CHOP activation acts as a pivotal trigger for ER stress-induced apoptosis. MicroRNA-616 is located within an intron of the CHOP gene. However, the regulation of miR-616 expression during UPR and its function in breast cancer is not clearly understood. Here we show that the expression of miR-616 and CHOP (host gene of miR-616) is downregulated in human breast cancer. Both miR-5p/-3p arms of miR-616 are expressed with levels of the 5p arm higher than the 3p arm. During conditions of ER stress, the expression of miR-616-5p and miR-616-3p arms was concordantly increased primarily through the PERK pathway. Our results show that ectopic expression of miR-616 significantly suppressed cell proliferation and colony formation, whereas knockout of miR-616 increased it. We found that miR-616 represses c-MYC expression via binding sites located in its protein coding region. Furthermore, we show that miR-616 exerted growth inhibitory effects on cells by suppressing c-MYC expression. Our results establish a new role for the CHOP locus by providing evidence that miR-616 can inhibit cell proliferation by targeting c-MYC. In summary, our results suggest a dual function for the CHOP locus, where CHOP protein and miR-616 can cooperate to inhibit cancer progression. Full article
(This article belongs to the Special Issue Apoptosis and Cell Signaling in Disease)
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15 pages, 8960 KiB  
Article
Sertindole, an Antipsychotic Drug, Curbs the STAT3/BCL-xL Axis to Elicit Human Bladder Cancer Cell Apoptosis In Vitro
by Chao-Yu Hsu, Wei-Ting Yang, Ju-Hwa Lin, Chien-Hsing Lu, Kai-Cheng Hu, Tsuo-Hung Lan and Chia-Che Chang
Int. J. Mol. Sci. 2023, 24(14), 11852; https://doi.org/10.3390/ijms241411852 - 24 Jul 2023
Cited by 3 | Viewed by 1761
Abstract
Bladder cancer is the leading urinary tract malignancy. Epidemiological evidence has linked lower cancer incidence in schizophrenia patients to long-term medication, highlighting the anticancer potential of antipsychotics. Sertindole is an atypical antipsychotic agent with reported anticancer action on breast and gastric cancers. Yet, [...] Read more.
Bladder cancer is the leading urinary tract malignancy. Epidemiological evidence has linked lower cancer incidence in schizophrenia patients to long-term medication, highlighting the anticancer potential of antipsychotics. Sertindole is an atypical antipsychotic agent with reported anticancer action on breast and gastric cancers. Yet, sertindole’s effect on bladder cancer remains unaddressed. We herein present the first evidence of sertindole’s antiproliferative effect and mechanisms of action on human bladder cancer cells. Sertindole was cytotoxic against bladder cancer cells while less cytotoxic to normal urothelial cells. Apoptosis was a primary cause of sertindole’s cytotoxicity, as the pan-caspase inhibitor z-VAD-fmk rescued cells from sertindole-induced killing. Mechanistically, sertindole inhibited the activation of signal transducer and activator of transcription 3 (STAT3), an oncogenic driver of bladder cancer, as sertindole lowered the levels of tyrosine 705-phosphorylated STAT3 along with that of STAT3′s target gene BCL-xL. Notably, ectopic expression of the dominant-active STAT3 mutant impaired sertindole-induced apoptosis in addition to restoring BCL-xL expression. Moreover, bladder cancer cells overexpressing BCL-xL were refractory to sertindole’s proapoptotic action, arguing that sertindole represses STAT3 to downregulate BCL-xL, culminating in the induction of apoptosis. Overall, the current study indicated sertindole exerts bladder cancer cytotoxicity by provoking apoptosis through targeted inhibition of the antiapoptotic STAT3/BCL-xL signaling axis. These findings implicate the potential to repurpose sertindole as a therapeutic strategy for bladder cancer. Full article
(This article belongs to the Special Issue Apoptosis and Cell Signaling in Disease)
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Review

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13 pages, 1667 KiB  
Review
Apoptosis Regulation in Osteoarthritis and the Influence of Lipid Interactions
by Frederike Werry, Emilia Mazur, Lars F. H. Theyse and Frank Edlich
Int. J. Mol. Sci. 2023, 24(17), 13028; https://doi.org/10.3390/ijms241713028 - 22 Aug 2023
Cited by 6 | Viewed by 1820
Abstract
Osteoarthritis (OA) is one of the most common chronic diseases in human and animal joints. The joints undergo several morphological and histological changes during the development of radiographically visible osteoarthritis. The most discussed changes include synovial inflammation, the massive destruction of articular cartilage [...] Read more.
Osteoarthritis (OA) is one of the most common chronic diseases in human and animal joints. The joints undergo several morphological and histological changes during the development of radiographically visible osteoarthritis. The most discussed changes include synovial inflammation, the massive destruction of articular cartilage and ongoing joint destruction accompanied by massive joint pain in the later stadium. Either the increased apoptosis of chondrocytes or the insufficient apoptosis of inflammatory macrophages and synovial fibroblasts are likely to underly this process. In this review, we discuss the current state of research on the pathogenesis of OA with special regard to the involvement of apoptosis. Full article
(This article belongs to the Special Issue Apoptosis and Cell Signaling in Disease)
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