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Biomedicines
Special Issues
Signaling Pathways That Regulate Cell Proliferation and Apoptosis
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Signaling Pathways That Regulate Cell Proliferation and Apoptosis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 3005

Special Issue Editor

Dr. Han Han

E-Mail Website
Guest Editor
Department of Developmental and Cell Biology, University of California, Irvine, Irvine, CA, USA
Interests: cell signaling pathways; cell homeostasis; protein–protein interactomes; gene regulation; cancer biology

Special Issue Information

Dear Colleagues,

A fundamental question in the growth of multicellular organisms is how the body knows to stop growing after reaching an adult age. When it comes to humans, in each adult, more than 50 billion cells die and are replaced by other cells every day, which means we change our entire body weight of cells every year. How can this happen? A simple answer is because of cell proliferation and apoptosis. Cell proliferation requires both cell growth and cell division to increase the cell size and population. Apoptosis is a form of programmed cell death which is induced by the inside death events of a cell. Both cell proliferation and apoptosis are required to maintain tissue hemostasis and normal growth. Therefore, the cell undergoing proliferation or apoptosis is tightly controlled by different biochemical signals. To receive, process, and transduce these signals, the cell develops a variety of cell signaling pathways to help the cell to function normally. However, loss of control of cell proliferation and apoptosis or dysregulation of these signaling pathways leads to a variety of diseases, including cancer. In this Special Issue, we call for a list of papers related to the signaling pathways that regulate cell proliferation and apoptosis under the context of either physiological or pathological conditions. We encourage the submissions of all article types, including but not limited to original research, review, systematic review, methods, perspectives, and communications within this specific topic.

Dr. Han Han
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cell proliferation
  • apoptosis
  • signaling pathway
  • signaling transduction
  • protein modification
  • gene regulation
  • cancer
  • other diseases

Published Papers (3 papers)

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Research

14 pages, 5032 KiB  
Article
Antiproliferative Activity of N-Acylhydrazone Derivative on Hepatocellular Carcinoma Cells Involves Transcriptional Regulation of Genes Required for G2/M Transition
by Amanda Aparecida Ribeiro Andrade, Fernanda Pauli, Carolina Girotto Pressete, Bruno Zavan, João Adolfo Costa Hanemann, Marta Miyazawa, Rafael Fonseca, Ester Siqueira Caixeta, Julia Louise Moreira Nacif, Alexandre Ferro Aissa, Eliezer J. Barreiro and Marisa Ionta
Biomedicines 2024, 12(4), 892; https://doi.org/10.3390/biomedicines12040892 - 18 Apr 2024
Viewed by 273
Abstract
Liver cancer is the second leading cause of cancer-related death in males. It is estimated that approximately one million deaths will occur by 2030 due to hepatic cancer. Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer subtype and is commonly diagnosed [...] Read more.
Liver cancer is the second leading cause of cancer-related death in males. It is estimated that approximately one million deaths will occur by 2030 due to hepatic cancer. Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer subtype and is commonly diagnosed at an advanced stage. The drug arsenal used in systemic therapy for HCC is very limited. Multikinase inhibitors sorafenib (Nexavar®) and lenvatinib (Lenvima®) have been used as first-line drugs with modest therapeutic effects. In this scenario, it is imperative to search for new therapeutic strategies for HCC. Herein, the antiproliferative activity of N-acylhydrazone derivatives was evaluated on HCC cells (HepG2 and Hep3B), which were chemically planned on the ALL-993 scaffold, a potent inhibitor of vascular endothelial growth factor 2 (VEGFR2). The substances efficiently reduced the viability of HCC cells, and the LASSBio-2052 derivative was the most effective. Further, we demonstrated that LASSBio-2052 treatment induced FOXM1 downregulation, which compromises the transcriptional activation of genes required for G2/M transition, such as AURKA and AURKB, PLK1, and CDK1. In addition, LASSBio-2052 significantly reduced CCNB1 and CCND1 expression in HCC cells. Our findings indicate that LASSBio-2052 is a promising prototype for further in vivo studies. Full article
(This article belongs to the Special Issue Signaling Pathways That Regulate Cell Proliferation and Apoptosis)
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20 pages, 12715 KiB  
Article
Vagal Stimulation Ameliorates Non-Alcoholic Fatty Liver Disease in Rats
by Hany A. Elkattawy, Samar Mortada Mahmoud, Ahmed El-Sayed Hassan, Ahmed Behiry, Hasnaa Ali Ebrahim, Ateya Megahed Ibrahim, Donia Elsaid Fathi Zaghamir, Mohamed El-Sherbiny and Sherein F. El-Sayed
Biomedicines 2023, 11(12), 3255; https://doi.org/10.3390/biomedicines11123255 - 08 Dec 2023
Viewed by 1011
Abstract
Background: The harmful consequences of non-alcoholic fatty liver disease (NAFLD) are posing an increasing threat to public health as the incidence of diabetes and obesity increases globally. A non-invasive treatment with a range of autonomic and metabolic benefits is transcutaneous vagus nerve stimulation [...] Read more.
Background: The harmful consequences of non-alcoholic fatty liver disease (NAFLD) are posing an increasing threat to public health as the incidence of diabetes and obesity increases globally. A non-invasive treatment with a range of autonomic and metabolic benefits is transcutaneous vagus nerve stimulation (tVNS). Aim of the study: To investigate the possible preventive impacts of VNS against adult rats’ NAFLD caused by a high-fat diet (HFD) and to clarify the underlying mechanisms. Methods: A total of thirty-two adult male rats were split into two groups: the HFD-induced NAFLD group (n = 24) and the control normal group (n = 8). The obesogenic diet was maintained for 12 weeks to induce hepatic steatosis. The HFD-induced NAFLD group (n = 24) was separated into three groups: the group without treatment (n = 8), the group with sham stimulation (n = 8), and the group with VNS treatment (n = 8). VNS was delivered for 30 min per day for 6 weeks after the establishment of NAFLD using a digital TENS device. The subsequent assessments included hepatic triglyceride, cholesterol content, serum lipid profile, and liver function testing. In this context, inflammatory biomarkers (TNF-α, IL-6) and hepatic oxidative stress (MDA, SOD, and GPx) were also assessed. To clarify the possible mechanisms behind the protective benefits of VNS, additional histological inspection and immunohistochemistry analysis of TNF-α and Caspase-3 were performed. Results: In the NAFLD-affected obese rats, VNS markedly decreased the rats’ body mass index (BMI) and abdominal circumference (AC). Liver function markers (albumin, ALT, and AST) and the serum lipid profile—which included a notable decrease in the amounts of hepatic triglycerides and cholesterol—were both markedly improved. Additionally, oxidative stress and inflammatory indicators showed a considerable decline with VNS. Notably, the liver tissues examined by histopathologists revealed that there is evidence of the protective impact of VNS on the oxidative and inflammatory states linked to HFD-induced NAFLD while maintaining the architectural and functional condition of the liver. Conclusions: Our findings suggest that VNS may represent a promising therapeutic candidate for managing NAFLD induced by obesity. It can be considered to be an effective adjuvant physiological intervention for the obese population with NAFLD to spare the liver against obesity-induced deleterious injury. Full article
(This article belongs to the Special Issue Signaling Pathways That Regulate Cell Proliferation and Apoptosis)
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22 pages, 3689 KiB  
Article
Regulation of Protein-Induced Apoptosis and Autophagy in Human Hepatocytes Treated with Metformin and Paclitaxel In Silico and In Vitro
by Norah Saeed Al-Zahrani, Mazin Abdulaziz Zamzami, Mohammed A. Baghdadi, Afnan H. El-Gowily and Ehab M. M. Ali
Biomedicines 2023, 11(10), 2688; https://doi.org/10.3390/biomedicines11102688 - 30 Sep 2023
Viewed by 1052
Abstract
Metformin and paclitaxel therapy offer promising outcomes in the treatment of liver cancer. Combining paclitaxel with metformin enhances treatment effectiveness and mitigates the adverse effects associated with paclitaxel alone. This study explored the anticancer properties of metformin and paclitaxel in HepG2 liver cancer [...] Read more.
Metformin and paclitaxel therapy offer promising outcomes in the treatment of liver cancer. Combining paclitaxel with metformin enhances treatment effectiveness and mitigates the adverse effects associated with paclitaxel alone. This study explored the anticancer properties of metformin and paclitaxel in HepG2 liver cancer cells, MCF-7 breast cancer cells, and HCT116 colon cancer cells. The results demonstrated that the combination of these agents exhibited a lower IC50 in the tested cell lines compared to paclitaxel monotherapy. Notably, treating the HepG2 cell line with this combination led to a reduction in the G0/G1 phase and an increase in the S and G2/M phases, ultimately triggering early apoptosis. To further investigate the interaction between the cellular proteins with paclitaxel and metformin, an in silico study was conducted using proteins chosen from a protein data bank (PDB). Among the proteins studied, AMPK-α, EGFRK, and FKBP12-mTOR exhibited the highest binding free energy, with values of −11.01, −10.59, and −15.63 kcal/mol, respectively, indicating strong inhibitory or enhancing effects on these proteins. When HepG2 cells were exposed to both paclitaxel and metformin, there was an upregulation in the gene expression of AMPK-α, a key regulator of the energy balance in cancer growth, as well as apoptotic markers such as p53 and caspase-3, along with autophagic markers including beclin1 and ATG4A. This combination therapy of metformin and paclitaxel exhibited significant potential as a treatment option for HepG2 liver cancer. In summary, the combination of metformin and paclitaxel not only enhances treatment efficacy but also reduces side effects. It induces cell cycle alterations and apoptosis and modulates key cellular proteins involved in cancer growth, making it a promising therapy for HepG2 liver cancer. Full article
(This article belongs to the Special Issue Signaling Pathways That Regulate Cell Proliferation and Apoptosis)
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