Expression of autocrine motility factor receptor in colorectal cancer as a predictor for disease recurrence

Despite substantial progress in cancer therapy, colorectal cancer (CRC) is still the third leading cause of cancer death worldwide, mainly due to the acquisition of resistance and disease recurrence in patients. Growing evidence indicates that deregulation of hormone signaling pathways and their cross-talk with other signaling cascades inside CRC cells may have an impact on therapy resistance. MicroRNAs (miRNAs) are small conserved non-coding RNAs thatfunction as negative regulators in many gene expression processes. Key studies have identified miRNA alterations in cancer progression and drug resistance. In this review, we provide a comprehensive overview and assessment of miRNAs role in hormone signaling pathways in CRC drug resistance and their potential as future targets for overcoming resistance to treatment.

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Hypoxia-inducible factor-1 drives the motility of the erythroid progenitor cell line, UT-7/Epo, via autocrine motility factor

Experimental Hematology ◽

10.1016/j.exphem.2005.01.013 ◽

2005 ◽

Vol 33 (5) ◽

pp. 531-541 ◽

Cited By ~ 6

Author(s):

Makoto Mikami ◽

Yoshito Sadahira ◽

Arayo Haga ◽

Takemi Otsuki ◽

Hideho Wada ◽

...

Keyword(s):

Cell Line ◽

Progenitor Cell ◽

Hypoxia Inducible Factor ◽

Autocrine Motility Factor ◽

Erythroid Progenitor ◽

Motility Factor ◽

Hypoxia Inducible Factor 1 ◽

Erythroid Progenitor Cell ◽

Progenitor Cell Line

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Clathrin-mediated endocytosis and recycling of autocrine motility factor receptor to fibronectin fibrils is a limiting factor for NIH-3T3 cell motility

Journal of Cell Science ◽

10.1242/jcs.113.18.3227 ◽

2000 ◽

Vol 113 (18) ◽

pp. 3227-3240 ◽

Cited By ~ 3

Author(s):

P.U. Le ◽

N. Benlimame ◽

A. Lagana ◽

A. Raz ◽

I.R. Nabi

Keyword(s):

Cell Surface ◽

Cell Motility ◽

Endocytic Pathway ◽

Limiting Factor ◽

Autocrine Motility Factor ◽

Endocytic Compartment ◽

Motility Factor ◽

Microtubule Disruption ◽

Nih 3T3 ◽

Fibronectin Fibrils

Autocrine motility factor receptor (AMF-R) is internalized via a clathrin-independent pathway to smooth endoplasmic reticulum tubules. This endocytic pathway is shown here to be inhibited by methyl-(beta)-cyclodextrin (m(beta)CD) implicating caveolae or caveolae-like structures in AMF internalization to smooth ER. AMF-R is also internalized via a clathrin-dependent pathway to a transferrin receptor-negative, LAMP-1/lgpA-negative endocytic compartment identified by electron microscopy as a multivesicular body (MVB). Endocytosed AMF recycles to cell surface fibrillar structures which colocalize with fibronectin; AMF-R recycling is inhibited at 20 degrees C, which blocks endocytosis past the early endosome, but not by m(beta)CD demonstrating that AMF-R recycling to fibronectin fibrils is mediated by clathrin-dependent endocytosis to MVBs. Microtubule disruption with nocodazole did not affect delivery of bAMF to cell surface fibrils indicating that recycling bAMF traverses the MVB but not a later endocytic compartment. Plating NIH-3T3 cells on an AMF coated substrate did not specifically affect cell adhesion but prevented bAMF delivery to cell surface fibronectin fibrils and reduced cell motility. AMF-R internalization and recycling via the clathrin-mediated pathway are therefore rate-limiting for cell motility. This recycling pathway to the site of deposition of fibronectin may be implicated in the de novo formation of cellular attachments or the remodeling of the extracellular matrix during cell movement.

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