FLO-1

Name: FLO-1
Brand: Creative Bioarray

Cat.No.: CSC-C9481J

Species: Homo sapiens (Human)

Source: Esophagus

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Cat.No.

CSC-C9481J

Description

FLO-1 was established from a primary distal oesophageal adenocarcinoma in a 68 year-old Caucasian male in 1991. The Y chromosome could not be detected in this cell line by short tandem repeat (STR)-PCR analysis. It is a known phenomenon that due to the increased genetic instability of cancer cell lines the Y chromosome can be rearranged or lost resulting in lack of detection.

Species

Homo sapiens (Human)

Source

Esophagus

Recommended Medium

DMEM + 2mM Glutamine + 10% Fetal Bovine Serum (FBS)

Disease

Barrett Adenocarcinoma

Storage

Liquid Nitrogen (-180 °C).

Storage and Shipping

Creative Bioarray ships frozen cells on dry ice. On receipt, immediately transfer frozen cells to liquid nitrogen (-180 °C) until ready for experimental use. Never can cryopreserved cells be kept at -20 °C.

Synonyms

Flo-1; Flo 1; FLO1; FLO

Citation Guidance

If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

FLO-1 is a continuous human esophageal adenocarcinoma (EAC) cell line derived from a primary distal esophageal adenocarcinoma, a tumor type frequently associated with Barrett’s esophagus. It exhibits epithelial morphology, adherent growth, and robust proliferation in standard culture, providing a reproducible and scalable in vitro model of EAC. FLO-1 cells express epithelial markers such as cytokeratins and E-cadherin, and are tumorigenic in immunodeficient mice, supporting subcutaneous and orthotopic xenograft studies.

Key advantages:

Human EAC relevance: Represents distal esophageal adenocarcinoma, a cancer with rising incidence and poor prognosis, and is useful for studying Barrett’s-associated carcinogenesis and EAC biology.
Experimental tractability: Amenable to transfection, siRNA/CRISPR perturbation, flow cytometry, immunostaining, qPCR, Western blot, and high-throughput drug screening.
In vivo compatibility: Supports xenograft models for tumor growth, metastasis, and treatment response.
Reproducibility: As a continuous line, it offers standardized culture, commercial availability, and reduced variability compared with primary tumors.

Applications: Chemoradiotherapy resistance, targeted therapy, invasion/metastasis, cancer stem cell biology, and biomarker discovery.

Non-Muscle Myosin Heavy Chain IIA Regulates Cell Morphology, Stress Fibre Structure, and Cell Migration in FLO-1 Oesophageal Adenocarcinoma Cells

Cell migration is tightly controlled in the healthy cell but can become dysregulated in diseases such as oesophageal adenocarcinoma (OAC) where increased cell motility and migration can contribute to metastasis. We investigated the role of an actin-based molecular motor, non-muscle myosin heavy chain IIA (NMHCIIA) in the migratory capacity of oesophageal adenocarcinoma cells.

Immunofluorescence microscopy and ratiometric imaging demonstrated that NMHCIIA co-localizes with F-actin at the leading edge and retracting rear of migrating FLO-1 OAC cells. siRNA-mediated depletion of NMHCIIA from FLO-1 cells altered cell morphology, gave rise to an increased number of stress fibre like structures and reduced FLO-1 cell migration. These findings suggest that NMHCIIA influences FLO-1 cell migration by regulating F-actin dynamics and the actin cytoskeleton, providing insight into the mechanisms of migration employed by OAC cells and identifying NMHCIIA as a potential therapeutic target for this disease.

NMHCIIA co-localizes with F-actin at the lamellipodial leading edge of migrating FLO-1 cells but does not co-localize with F-actin at the leading edge of migrating SKGT-4 cells. — Fig. 1. NMHCIIA co-localizes with F-actin at the lamellipodial leading edge of migrating FLO-1, but not SKGT-4, cells (Duff, Deirdre, Siobhan Gargan, and Aideen Long. 2025).

NMHCIIA depletion alters FLO-1 cell morphology and F-actin organization. — Fig. 2. NMHCIIA depletion alters FLO-1 cell morphology and F-actin organization (Duff, Deirdre, Siobhan Gargan, and Aideen Long. 2025).

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