Tumors comprise diverse cancer cell populations with specific capabilities for adaptation to the tumor microenvironment, resistance to anticancer treatments, and metastatic dissemination. However, whether these populations are pre-existing in cancer cells or stochastically appear during tumor growth remains unclear. Here, we show the heterogeneous behaviors of cancer cells regarding response to anticancer drug treatments, formation of lung metastases, and expression of transcription factors related to cancer stem-like cells using a DNA barcoding and gene expression recording system. B16F10 cells maintained clonal diversity after treatment with HVJ-E, a UV-irradiated Sendai virus, and the anticancer drug dacarbazine. PBS treatment of the primary tumor and intravenous injection of B16F10 cells resulted in metastases formed from clones of multiple cell lineages. Conversely, BL6 and 4T1 cells developed spontaneous lung metastases by a small number of clones. Notably, an identical clone of 4T1 cells developed lung metastases in different mice, suggesting the existence of cells with high metastatic potential. Cas9-based transcription recording analysis in a human prostate cancer cell line revealed that specific cells express POU5F1 in response to an anticancer drug and sphere formation. Our findings provide insights into the diversity of cancer cells during tumor progression.
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http://dx.doi.org/10.1007/s00018-022-04640-4 | DOI Listing |
Int J Biol Markers
January 2025
Department of Respiratory and Critical Care Medicine, Anyue County People's Hospital, Anyue, China.
Purpose: To detect the prognostic importance of liquid-liquid phase separation (LLPS) in lung adenocarcinoma.
Methods: The gene expression files, copy number variation data, and clinical data were downloaded from The Cancer Genome Atlas cohort. LLPS-related genes were acquired from the DrLLPS website.
Asia Pac J Clin Oncol
January 2025
Department of Thyroid and Breast Surgery, The Second Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Aim: Breast cancer (BC) is the most frequently diagnosed malignancy worldwide, necessitating continued research into its molecular mechanisms. Circular RNAs (circRNAs) are increasingly recognized for their role in various cancers, including BC. This study explores the role of circRNA kinesin family member 4A (circKIF4A) in BC progression and its underlying molecular mechanisms.
View Article and Find Full Text PDFCA Cancer J Clin
January 2025
Division of Medical Oncology, Department of Internal Medicine, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, USA.
Poly(adenosine diphosphate ribose) polymerase (PARP) inhibitors, such as olaparib, talazoparib, rucaparib, and niraparib, comprise a therapeutic class that targets PARP proteins involved in DNA repair. Cancer cells with homologous recombination repair defects, particularly BRCA alterations, display enhanced sensitivity to these agents because of synthetic lethality induced by PARP inhibitors. These agents have significantly improved survival outcomes across various malignancies, initially gaining regulatory approval in ovarian cancer and subsequently in breast, pancreatic, and prostate cancers in different indications.
View Article and Find Full Text PDFChembiochem
January 2025
Ludwig-Maximilians-Universitat Munchen, Chemistry, Butenandstr. 5-13, 81377, Muenchen, GERMANY.
In the last decade the important role of small non-coding RNAs such as micro RNAs (miRs) in gene regulation in healthy and disease states became more and more evident. The miR-200-family of miRs has been shown to play a critical role in many diseases such as cancer and neurodegenerative disorders and could be potentially important for diagnosis and treatment. However, the size of miRs of about ~21-23nt provide challenges for their investigation.
View Article and Find Full Text PDFOncol 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.
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