Anoikis, a form of programmed cell death triggered by detachment from the extracellular matrix (ECM), maintains tissue homeostasis by removing mislocalized or detached cells. Cancer cells, however, have evolved multiple mechanisms to evade anoikis under conditions of ECM detachment, enabling survival and distant metastasis. Studies have identified differentially expressed proteins between suspended and adherent cancer cells, revealing that key metabolic and signaling pathways undergo significant alterations during the acquisition of anoikis resistance. This review explores the regulatory roles of epithelial-mesenchymal transition, cancer stem cell characteristics, metabolic reprogramming, and various signaling pathway alterations in promoting anoikis resistance. And the corresponding reagents and non-coding RNAs that target the aforementioned pathways are reviewed. By discussing the regulatory mechanisms that facilitate anoikis resistance in cancer cells, this review aims to shed light on potential strategies for inhibiting tumor progression and preventing metastasis.
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http://dx.doi.org/10.1007/s11010-024-05199-3 | DOI Listing |
Cell Signal
January 2025
State Key Laboratory of Analytical Chemistry for Life Science, Division of Anatomy and Histo-embryology, Medical School, Nanjing University, Nanjing, Jiangsu 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing, Jiangsu 210093, China. Electronic address:
Autophagy-mediated anoikis resistance plays a critical role in the initiation of tumor metastasis. Therefore, we investigated the role and mechanism of anoikis resistance mediated by free fatty acids (FFAs) derived from lipophagy in highly invasive clear cell renal cell carcinoma (ccRCC). Here, we found that the highly invasive ccRCC cell line Himi exhibited enhanced resistance to anoikis and elevated lipophagy levels.
View Article and Find Full Text PDFMol Cell Biochem
January 2025
Department of Nursing, Operating Room, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Anoikis, a form of programmed cell death triggered by detachment from the extracellular matrix (ECM), maintains tissue homeostasis by removing mislocalized or detached cells. Cancer cells, however, have evolved multiple mechanisms to evade anoikis under conditions of ECM detachment, enabling survival and distant metastasis. Studies have identified differentially expressed proteins between suspended and adherent cancer cells, revealing that key metabolic and signaling pathways undergo significant alterations during the acquisition of anoikis resistance.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Cancer Research UK Scotland Centre (Edinburgh), Institute of Genetics & Cancer, University of Edinburgh, Edinburgh, UK.
E-cadherin is a transmembrane protein and central component of adherens junctions (AJs). The extracellular domain of E-cadherin forms homotypic interactions with E-cadherin on adjacent cells, facilitating the formation of cell-cell adhesions, known as AJs, between neighbouring cells. The intracellular domain of E-cadherin interacts with α-, β- and p120-catenins, linking the AJs to the actin cytoskeleton.
View Article and Find Full Text PDFJ Pathol
January 2025
Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, PR China.
Aberrant expression of grainyhead-like transcription factor 3 (GRHL3) has been extensively reported in the development and progression of several squamous cell carcinomas, such as cutaneous, head and neck, and esophageal squamous cell carcinoma. However, the clinical significance and biological roles of GRHL3 in lung squamous cell (LUSC) carcinoma are largely unclear. Herein, we report that GRHL3 was significantly upregulated in lung squamous epithelium of LUSC tissues, bronchiole, and bronchus.
View Article and Find Full Text PDFBiomed Rep
March 2025
Department of Biology, Xavier University of Louisiana, New Orleans, LA 70125, USA.
As a putative lung specific oncogene, the transducin-like enhancer of split 1 (TLE1) corepressor drives an anti-apoptotic and pro-epithelial-mesenchymal transition (EMT) gene transcriptional programs in human lung adenocarcinoma (LUAD) cells, thereby promoting anoikis resistance and tumor aggressiveness. Through its survival- and EMT-promoting gene regulatory programs, TLE1 may impact drug sensitivity and resistance in lung cancer cells. In the present study, a novel function of TLE1 was uncovered as an inhibitor of the antitumor effects of the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) gefitinib in the human LUAD cell line A549, which exhibits moderate sensitivity to EGFR-TKI.
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