Concomitant Alterations of Microfilaments and Microtubules in Human Epithelial Cells (HBL-100) in Relation to Their Malignant Conversion

Abstract

The organization of microfilaments and microtubules was studied in human epithelial HBL-100 cells at different steps in their malignant conversion. This conversion was obtained either spontaneously upon successive in vitro subcultures (∼ p. 70), or after superinfection of early passage non-tumorigenic cells (p. 28) with Kirsten murine sarcoma virus. Our results point out a clear relationship between the progression of cells toward malignancy, whatever the modality of malignant transformation, and severe cytoskeleton modifications. The fragmentation of F-actin fibers was the earliest event occurring at p. 46, before the appearance of tumorigenicity. In tumorigenic cells, intracytoplasmic F-actin was nearly completely fragmented, the bundle of peripheral actin was loosened and poorly stained whereas the tubulin network was more important and more largely extended throughout the cytoplasm than in non tumorigenic cells.

A pan-cancer analysis of the prognostic and immunological role of β-actin (ACTB) in human cancers

“…ACTB is an essential component of cytoskeleton playing a critical role in cell growth and cell migration [5,63], and ACTB was significantly overexpressed in different tumor cell lines of highly invasive ability [9]. The polymerization and remolding of the ACTB could regulate the morphology and phenotype of malignant cells and contribute to tumor malignancy [64][65][66][67]. We speculated that ACTB upregulation in cancers might regulate tumor cell proliferation, phenotype and metastasis to further influence the tumor malignancy and prognosis of tumor patients.…”

Chemotherapeutic drugs change actin skeleton organization and the expression of β-thymosins in human breast cancer cells

“…Cell transformation, reflecting a step in tumorigenesis, is accompanied by a loss of growth regulation as well as by changes in cell morphology, reduced cell-cell contact and substrate adhesion, and, in particular, by a loss of actin filaments (Decloitre et al 1991). Even though the precise mechanisms of how actin is involved in tumorigenic transformation are not yet completely delineated, it is becoming evident that a myriad of actin-binding proteins governing the organization of the actin structures is involved (Pollard 1986;Kreis and Vale 1993).…”

Thymosin β4 targeting impairs tumorigenic activity of colon cancer stem cells

“…C ell transformation is accompanied by a loss of actin filaments that contribute to alter cell morphology and reduce cell‐cell contact and adhesion (1). Even though the precise mechanisms of how actin is involved in cancer transformation are not yet well understood, the involvement in the tumorigenic process of a series of actin‐binding proteins that govern the organization of the actin structures is becoming evident.…”