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Molecular Advances in Cell Proliferation, Senescence and Apoptosis

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 September 2025 | Viewed by 4682

Special Issue Editor


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Guest Editor
Department of Surgery, University of Virginia School of Medicine, Charlottesville, VA 22903, USA
Interests: cell survival; apoptosis; cell proliferation; senescence; progenitor cells; cancer; heart failure; long noncoding RNA
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Special Issue Information

Dear Colleagues,

Biological molecules, including carbohydrates, lipids, proteins, and nucleic acids, are the building blocks of life. Carbohydrates provide energy and structure, lipids store energy and form cell membranes, proteins perform various functions and catalyse reactions, and nucleic acids store and transfer genetic information. The field of molecular biology has seen significant advances in our understanding of cell proliferation, senescence, and apoptosis. These processes play critical roles in normal tissue development, homeostasis, and diseases. Cell proliferation, the process of increasing the number of cells by cell division and cell growth, is regulated by a complex network of genes and proteins that control the cell cycle and respond to external signals. Cellular senescence, a phenomenon characterized by the cessation of cell division, can be initiated by a wide variety of stress-inducing molecules, including factors related to abnormal cellular growth, oxidative stress, and autophagy. Cell apoptosis, a form of programmed cell death, is a highly regulated and controlled process that confers advantages during an organism's life cycle. Gain, loss, or mutation of critical biological molecules have been widely associated with the dysregulation of cell proliferation, senescence, and apoptosis; they thus have significant impacts on the progression of human diseases, including cancer, diabetes, neurodegenerative diseases, and cardiovascular diseases.

This Special Issue focuses on the discovery of biological molecules that control cell proliferation, senescence, and apoptosis. Original papers, reviews articles, and perspectives from experts in this field are welcome.

Dr. Chuanxi Cai
Guest Editor

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Keywords

  • biological molecules
  • cell proliferation
  • senescence
  • apoptosis
  • human diseases

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Published Papers (3 papers)

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Research

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10 pages, 26791 KiB  
Article
The Antiproliferative and Proapoptotic Effects of Cucurbitacin B on BPH-1 Cells via the p53/MDM2 Axis
by Ping Zhou, Sisi Huang, Congcong Shao, Dongyan Huang, Yingyi Hu, Xin Su, Rongfu Yang, Juan Jiang and Jianhui Wu
Int. J. Mol. Sci. 2024, 25(1), 442; https://doi.org/10.3390/ijms25010442 - 28 Dec 2023
Cited by 3 | Viewed by 1536
Abstract
Cucurbitacin B (Cu B), a triterpenoid compound, has anti-inflammatory and antioxidant activities. Most studies only focus on the hepatoprotective activity of Cu B, and little effort has been geared toward exploring the effect of Cu B on the prostate. Our study identified that [...] Read more.
Cucurbitacin B (Cu B), a triterpenoid compound, has anti-inflammatory and antioxidant activities. Most studies only focus on the hepatoprotective activity of Cu B, and little effort has been geared toward exploring the effect of Cu B on the prostate. Our study identified that Cu B inhibited the proliferation of the benign prostatic hyperplasia epithelial cell line (BPH-1). At the molecular level, Cu B upregulated MDM2 and thrombospondin 1 (THBS1) mRNA levels. Immunocytochemistry results revealed that the protein expressions of p53 and MDM2 were upregulated in BPH-1 cells. Furthermore, Cu B upregulated THBS1 expression and downregulated COX-2 expression in the BPH-1 cell supernatant. Altogether, Cu B may inhibit prostate cell proliferation by activating the p53/MDM2 signaling cascade and downregulating the COX-2 expression. Full article
(This article belongs to the Special Issue Molecular Advances in Cell Proliferation, Senescence and Apoptosis)
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17 pages, 5418 KiB  
Article
SOX18 Promotes the Proliferation of Dermal Papilla Cells via the Wnt/β-Catenin Signaling Pathway
by Mingliang He, Xiaoyang Lv, Xiukai Cao, Zehu Yuan, Tesfaye Getachew, Yutao Li, Shanhe Wang and Wei Sun
Int. J. Mol. Sci. 2023, 24(23), 16672; https://doi.org/10.3390/ijms242316672 - 23 Nov 2023
Cited by 1 | Viewed by 1658
Abstract
SRY-box transcription factor 18 (SOX18) is known to play a crucial role in the growth and development of hair follicles (HF) in both humans and mice. However, the specific effect of SOX18 on sheep hair follicles remains largely unknown. In our [...] Read more.
SRY-box transcription factor 18 (SOX18) is known to play a crucial role in the growth and development of hair follicles (HF) in both humans and mice. However, the specific effect of SOX18 on sheep hair follicles remains largely unknown. In our previous study, we observed that SOX18 was specifically expressed within dermal papilla cells (DPCs) in ovine hair follicles, leading us to investigate its potential role in the growth of hair follicles in sheep. In the present study, we aimed to examine the effect of SOX18 in DPCs and preliminarily study its regulatory mechanism through RNA-seq. We initially found that the overexpression of SOX18 promoted the proliferation of DPCs compared to the negative control group, while the interference of SOX18 had the opposite effect. To gain further insight into the regulatory mechanism of SOX18, we conducted RNA-seq analysis after knocking down SOX18 in Hu sheep DPCs. The result showed that the Wnt/β-Catenin signaling pathway was involved in the growth process of DPC after SOX18 knockdown. Subsequently, we investigated the effect of SOX18 on the Wnt/β-Catenin signaling pathway in DPCs using TOP/FOP-flash, qRT-PCR, and Western blot (WB) analysis. Our data demonstrated that SOX18 could activate the Wnt/β-Catenin signaling pathway in DPCs. Additionally, we observed that SOX18 could rescue the proliferation of DPCs after inhibiting the Wnt/β-Catenin signaling pathway. These findings underscore the essential role of SOX18 as a functional molecule governing the proliferation of DPCs. Additionally, these findings also greatly enhance our understanding of the role of SOX18 in the proliferation of DPCs and the growth of wool in Hu sheep. Full article
(This article belongs to the Special Issue Molecular Advances in Cell Proliferation, Senescence and Apoptosis)
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Review

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34 pages, 1309 KiB  
Review
Bid Protein: A Participant in the Apoptotic Network with Roles in Viral Infections
by Zbigniew Wyżewski, Karolina Paulina Gregorczyk-Zboroch, Matylda Barbara Mielcarska, Weronika Świtlik and Adrianna Niedzielska
Int. J. Mol. Sci. 2025, 26(6), 2385; https://doi.org/10.3390/ijms26062385 - 7 Mar 2025
Viewed by 693
Abstract
The BH3-interacting domain death agonist (Bid), a proapoptotic signaling molecule of the B-cell lymphoma 2 (Bcl-2) family, is a key regulator of mitochondrial outer membrane (MOM) permeability. Uniquely positioned at the intersection of extrinsic and intrinsic apoptosis pathways, Bid links death receptor signaling [...] Read more.
The BH3-interacting domain death agonist (Bid), a proapoptotic signaling molecule of the B-cell lymphoma 2 (Bcl-2) family, is a key regulator of mitochondrial outer membrane (MOM) permeability. Uniquely positioned at the intersection of extrinsic and intrinsic apoptosis pathways, Bid links death receptor signaling to the mitochondria-dependent cascade and can also be activated by endoplasmic reticulum (ER) stress. In its active forms, cleaved Bid (cBid) and truncated Bid (tBid), it disrupts MOM integrity via Bax/Bak-dependent and independent mechanisms. Apoptosis plays a dual role in viral infections, either promoting or counteracting viral propagation. Consequently, viruses modulate Bid signaling to favor their replication. The deregulation of Bid activity contributes to oncogenic transformation, inflammation, immunosuppression, neurotoxicity, and pathogen propagation during various viral infections. In this work, we explore Bid’s structure, function, activation processes, and mitochondrial targeting. We describe its role in apoptosis induction and its involvement in infections with multiple viruses. Additionally, we discuss the therapeutic potential of Bid in antiviral strategies. Understanding Bid’s signaling pathways offers valuable insights into host–virus interactions and the pathogenesis of infections. This knowledge may facilitate the development of novel therapeutic approaches to combat virus-associated diseases effectively. Full article
(This article belongs to the Special Issue Molecular Advances in Cell Proliferation, Senescence and Apoptosis)
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