Colony formation is an essential stage of cyanobacterial blooms. High calcium concentration can promote Microcystis aeruginosa aggregation behavior, but the mechanism of colony formation caused by calcium has rarely been reported. In this study, high calcium-induced colony formation was identified as a shift from cell adhesion to cell division, rather than only cell adhesion as previously thought. Algae responded to this calcium-induced environmental pressure by aggregating and forming colonies. Algal cells initially secreted large quantities of extracellular polysaccharides (EPS) and rapidly aggregated by cell adhesion. The highest aggregation proportion was up to 68.93%. However, high calcium concentrations cannot completely inhibit algal cell growth, but only delay the algae into the rapid growth phase. With adaption to calcium and existing high EPS content, the daughter cells reduced EPS synthesis and the aggregation proportion decreased. The increasing growth rate was also responsible for the decreased xylose content in EPS. The mechanism of colony formation changed to cell division. The downregulation of genes related to EPS secretion also supported this hypothesis. Overall, these results can benefit for our understanding of cyanobacterial bloom formation.
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http://dx.doi.org/10.1016/j.envpol.2022.119997 | DOI Listing |
Oncol Res
December 2024
Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Background: Triple-negative breast cancer (TNBC), characterized by its lack of traditional hormone receptors and HER2, presents a significant challenge in oncology due to its poor response to conventional therapies. Autophagy is an important process for maintaining cellular homeostasis, and there are currently autophagy biomarkers that play an effective role in the clinical treatment of tumors. In contrast to targeting protein activity, intervention with protein-protein interaction (PPI) can avoid unrelated crosstalk and regulate the autophagy process with minimal interference pathways.
View Article and Find Full Text PDFOncol Res
December 2024
Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Objective: Gastric cancer (GC) is a globally common cancer characterized by high incidence and mortality worldwide. Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy. Long non-coding RNAs (lncRNAs) and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies.
View Article and Find Full Text PDFFront Oncol
December 2024
Department of Orthopedics, Chengdu Fifth People's Hospital, Chengdu, China.
Background: Prostate cancer (PCa) ranks as the second leading cause of cancer-related mortality among men. Long non-coding RNAs (lncRNAs) are known to play a regulatory role in the development of various human cancers. LncRNA MAFG-divergent transcript (MAFG-DT) was reported to play a crucial role in tumor progression of multiple human cancers, such as pancreatic cancer, colorectal cancer, bladder cancer, and gastric cancer.
View Article and Find Full Text PDFPeerJ
December 2024
Medical Oncology, Inner Mongolia People's Hospital, Hohhot, China.
Background: CLP36 is also known as PDZ and LIM Domain 1 (PDLIM1) that is a ubiquitously-expressed α-actinin-binding cytoskeletal protein involved in carcinogenesis, and our current study aims to explore its involvement in lymphoma.
Methods: Accordingly, the CLP36 expression pattern in lymphoma and its association with the overall survival was predicted. Then, qPCR was applied to gauge CLP36 expression in lymphoma cells and determine the knockdown efficiency.
World J Gastroenterol
December 2024
Department of Gastroenterology and Hepatology, The First Medical Center, Chinese People's Liberation Army General Hospital, Beijing 100853, China.
Background: Hepatocellular carcinoma (HCC) is a prevalent and aggressive tumor. Sorafenib is the first-line treatment for patients with advanced HCC, but resistance to sorafenib has become a significant challenge in this therapy. Cancer stem cells play a crucial role in sorafenib resistance in HCC.
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