Vimentin-mediated regulation of cell motility through modulation of beta4 integrin protein levels in oral tumor derived cells

Dmello, Crismita; Sawant, Sharada; Alam, Hunain; Gangadaran, Prakash; Tiwari, Richa; Dongre, Harsh; Rana, Neha; Barve, Sai; Costea, Daniela Elena; Chaukar, Davendra; Kane, Shubhada; Pant, Harish C.; Vaidya, Milind M.

doi:10.1016/j.biocel.2015.11.015

Cited by 32 publications

(41 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in a study using oral squamous cell carcinoma cells, authors showed that knock-down of vimentin leads to an increase in β4-integrin levels, and a more adherent behavior when cells were grown on laminin-5. No change in adhesion was observed on fibronectin [31]. These observations, therefore, suggest that the function of vimentin in FAs might be dependent on cell type and the ECM substrate.…”

Section: Vimentin In Focal Adhesionsmentioning

confidence: 56%

“…In keratinocytes, the reconstitution of vimentin in vimentin knock-out cells was sufficient to restore ERK1/2 signaling [30]. However, in a Cancers 2020, 12, 184 3 of 20 different study where cells were plated on laminin-5, the ERK pathway was unaffected after vimentin knock-down [31].…”

Section: Vimentin In Emtmentioning

confidence: 99%

“…Human mammary epithelial cells MCF10A were found to express vimentin in a wound-healing experiment at the wound's edge in actively migrating cells [71]. Vimentin was also proved to be important in wound-healing assays in works using other cell lines [31,64,72]. Moreover, vimentin knock-down in the lung cancer cell line A549 led to slower and less directed migration.…”

Section: Vimentin In Migration and Invasionmentioning

confidence: 99%

“…Moreover, vimentin knock-down in the lung cancer cell line A549 led to slower and less directed migration. Similarly, oral squamous cell carcinoma cells formed fewer colonies in soft agar and were less capable of invading Matrigel upon vimentin knock-down [31]. Vimentin deficiency in mice resulted in impaired wound healing [73].…”

Section: Vimentin In Migration and Invasionmentioning

confidence: 99%

“…Cancers 2019, 11, x FOR PEER REVIEW 3 of 21 3 reconstitution of vimentin in vimentin knock-out cells was sufficient to restore ERK1/2 signaling [30]. However, in a different study where cells were plated on laminin-5, the ERK pathway was unaffected after vimentin knock-down [31]. Taken together, these results place vimentin at the very center of the whole EMT process-both downstream and upstream of major metastatic progression drivers-creating a feedback loop actively supporting the pro-migratory properties of cells (Figure 1).…”

mentioning

confidence: 99%

See 4 more Smart Citations

Vimentin Intermediate Filaments as Potential Target for Cancer Treatment

Strouhalova

Přechová

Gandalovičová

et al. 2020

Cancers

188

143

View full text Add to dashboard Cite

Intermediate filaments constitute the third component of the cellular skeleton. Unlike actin and microtubule cytoskeletons, the intermediate filaments are composed of a wide variety of structurally related proteins showing distinct expression patterns in tissues and cell types. Changes in the expression patterns of intermediate filaments are often associated with cancer progression; in particular with phenotypes leading to increased cellular migration and invasion. In this review we will describe the role of vimentin intermediate filaments in cancer cell migration, cell adhesion structures, and metastasis formation. The potential for targeting vimentin in cancer treatment and the development of drugs targeting vimentin will be reviewed.

show abstract

Section: Vimentin In Focal Adhesionsmentioning

confidence: 56%

Section: Vimentin In Emtmentioning

confidence: 99%

Section: Vimentin In Migration and Invasionmentioning

confidence: 99%

Section: Vimentin In Migration and Invasionmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Vimentin Intermediate Filaments as Potential Target for Cancer Treatment

Strouhalova

Přechová

Gandalovičová

et al. 2020

Cancers

188

143

View full text Add to dashboard Cite

show abstract

FKBP1A upregulation correlates with poor prognosis and increased metastatic potential of HNSCC

Patel

Dabhi

Dmello

et al. 2021

Cell Biology International

Self Cite

View full text Add to dashboard Cite

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy globally. The etiology of HNSCC is multifactorial, including cellular stress induced by a tobacco smoking, tobacco chewing excess alcohol consumption, and human papillomavirus infection. The induction of stress includes autophagy as one of the response pathways in maintaining homeostatic equilibrium. We evaluated the expression of autophagy‐related genes in HNSCC tissues from RNA sequencing datasets and identified 19 genes correlated with poor prognosis and 18 genes correlated with improved prognosis of HNSCC patients. Further analysis of independent gene expression datasets revealed that ATG12, HSP90AB1, and FKBP1A are overexpressed in HNSCC and correlate with poor prognosis, whereas the overexpression of ANXA1, FOS, and ULK3 correlates with improved prognosis. Using independent datasets, we also found that ATG12, HSP90AB1, and FKBP1A expression increased with an increase in the T‐stage of HNSCC. Among all the datasets analyzed, FKBP1A was overexpressed in HNSCC and was strongly associated with lymph node metastasis in multiple in silico datasets. In conclusion, our analysis indicates dynamic alterations in autophagy genes during HNSCC and warrants further investigation, specifically on FKBP1A and its role in tumor progression and metastasis.

show abstract

Mechanotransduction and epigenetic modulations of chromatin: Role of mechanical signals in gene regulation

Mishra,

Chakraborty,

Niharika

et al. 2024

J of Cellular Biochemistry

View full text Add to dashboard Cite

Mechanical forces may be generated within a cell due to tissue stiffness, cytoskeletal reorganization, and the changes (even subtle) in the cell's physical surroundings. These changes of forces impose a mechanical tension within the intracellular protein network (both cytosolic and nuclear). Mechanical tension could be released by a series of protein–protein interactions often facilitated by membrane lipids, lectins and sugar molecules and thus generate a type of signal to drive cellular processes, including cell differentiation, polarity, growth, adhesion, movement, and survival. Recent experimental data have accentuated the molecular mechanism of this mechanical signal transduction pathway, dubbed mechanotransduction. Mechanosensitive proteins in the cell's plasma membrane discern the physical forces and channel the information to the cell interior. Cells respond to the message by altering their cytoskeletal arrangement and directly transmitting the signal to the nucleus through the connection of the cytoskeleton and nucleoskeleton before the information despatched to the nucleus by biochemical signaling pathways. Nuclear transmission of the force leads to the activation of chromatin modifiers and modulation of the epigenetic landscape, inducing chromatin reorganization and gene expression regulation; by the time chemical messengers (transcription factors) arrive into the nucleus. While significant research has been done on the role of mechanotransduction in tumor development and cancer progression/metastasis, the mechanistic basis of force‐activated carcinogenesis is still enigmatic. Here, in this review, we have discussed the various cues and molecular connections to better comprehend the cellular mechanotransduction pathway, and we also explored the detailed role of some of the multiple players (proteins and macromolecular complexes) involved in mechanotransduction. Thus, we have described an avenue: how mechanical stress directs the epigenetic modifiers to modulate the epigenome of the cells and how aberrant stress leads to the cancer phenotype.

show abstract

Vimentin-mediated regulation of cell motility through modulation of beta4 integrin protein levels in oral tumor derived cells

Cited by 32 publications

References 46 publications

Vimentin Intermediate Filaments as Potential Target for Cancer Treatment

Vimentin Intermediate Filaments as Potential Target for Cancer Treatment

FKBP1A upregulation correlates with poor prognosis and increased metastatic potential of HNSCC

Mechanotransduction and epigenetic modulations of chromatin: Role of mechanical signals in gene regulation

Contact Info

Product

Resources

About