Antibiotics are classically perceived as biological weapons that bacteria produce to hold their ground against competing species in their natural habitat. But in the context of multicellular differentiation processes, antimicrobial compounds sometimes also play a role in intraspecies competition, resulting in the death of a sub-population of genetically identical siblings for the benefit of the population. Such a strategy is based on the diversification and hence phenotypic heterogeneity of an isogenic bacterial population. This review article will address three such phenomena. In Bacillus subtilis, cannibalism is a differentiation strategy that enhances biofilm formation, prolongs or potentially even prevents full commitment to endospore formation under starvation conditions, and protects cells within the biofilm against competing species. The nutrients released by lysed cells can be used by the toxin producers, thereby delaying the full activation of the master regulator of sporulation. A related strategy is associated with the initiation of competence development under nutrient excess in Streptococcus pneumoniae. This process, termed fratricide, causes allolysis in a sub-population and is thought to enhance genetic diversity within the species. In Myxococcus xanthus, a large fraction of the population undergoes programmed cell death during the formation of fruiting bodies. This sacrifice ensures the survival of the sporulating sub-population by providing nutrients and hence energy to complete this differentiation process. The biological relevance and underlying regulatory mechanisms of these three processes will be discussed in order to extract common features of such strategies. Moreover, open questions and future challenges will be addressed.
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http://dx.doi.org/10.1016/j.jmb.2019.04.024 | DOI Listing |
Oncol Rep
March 2025
Graduate Institute of Nanomedicine and Medical Engineering, College of Medical Engineering, Taipei Medical University, Taipei 11031, Taiwan, R.O.C.
Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells.
View Article and Find Full Text PDFInt J Oncol
February 2025
Department of Pathology, GROW Research Institute for Oncology and Reproduction, Maastricht University Medical Center, 6229HX Maastricht, The Netherlands.
Human papillomavirus (HPV)‑positive and -negative head and neck squamous cell carcinoma (HNSCC) are often associated with activation of the phosphatidylinositol 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway due to mutations or amplifications in , loss of or activation of receptor tyrosine kinases. In HPV‑negative tumors, (encoding p16 protein) inactivation or (encoding Cyclin D1 protein) amplification frequently results in sustained cyclin‑dependent kinase (CDK) 4/6 activation. The present study aimed to investigate the efficacy of the CDK4/6 inhibitors (CDKi) palbociclib and ribociclib, and the PI3K/Akt/mTOR pathway inhibitors (PI3Ki) gedatolisib, buparlisib and alpelisib, in suppressing cell viability of HPV‑positive and ‑negative HNSCC cell lines.
View Article and Find Full Text PDFMol Med Rep
March 2025
State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, SAR 999078, P.R. China.
Subarachnoid hemorrhage (SAH), a prevalent cerebrovascular condition associated with a high mortality rate, frequently results in neuronal apoptosis and an unfavorable prognosis. The adjunctive use of traditional Chinese medicine (TCM) with surgical interventions exerts a therapeutic impact on SAH, potentially by facilitating apoptosis. However, the mechanism by which TCM mediates apoptosis following SAH remains unclear.
View Article and Find Full Text PDFMol Med Rep
March 2025
The First Central Clinical School, Tianjin Medical University, Tianjin 300000, P.R. China.
Hepatocellular carcinoma (HCC) is a common cause of cancer‑related mortality and morbidity worldwide. While iodine‑125 (I) particle brachytherapy has been extensively used in the clinical treatment of various types of cancer, the precise mechanism underlying its effectiveness in treating HCC remains unclear. In the present study, MHCC‑97H cells were treated with I, after which, cell viability and proliferation were assessed using Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine and colony formation assays, cell invasion and migration were evaluated using wound healing and Transwell assays, and cell apoptosis was determined using flow cytometry.
View Article and Find Full Text PDFEndocr Metab Immune Disord Drug Targets
January 2025
Department of Orthopaedic Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Background: Osteoporosis (OP) is a skeletal condition characterized by increased susceptibility to fractures. Programmed cell death (PCD) is the orderly process of cells ending their own life that has not been thoroughly explored in relation to OP.
Objective: This study is to investigate PCD-related genes in OP, shedding light on potential mechanisms underlying the disease.
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