Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Retinoic acid negatively regulates beta 4 integrin expression and suppresses the malignant phenotype in a Lewis lung carcinoma cell line.

Clinical & experimental metastasis - 1 Jan 1994

Gaetano C, Melchiori A, Albini A, Benelli R, Falcioni R, Modesti A, Modica A, Scarpa S, Sacchi A

Abstract excerpt

Retinoic acid (RA) is a potent inhibitor of the malignant phenotype and of tumour cell growth. We observed that in vitro RA treatment of a highly metastatic lung carcinoma cell line (C87) induced a marked reduction in the amount of the beta 4 integrin subunit. The downregulation of this adhesion molecule was assessed by immunofluorescence, immunoprecipitation, and northern analysis. In order to investigate the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Differentiation
Share to DNA

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Lung Neoplasms

Share to Mice, Inbred C57BL

Share to Neoplasms, Experimental

Share to Phenotype

Share to Tumor Cells, Cultured

Source

Identifiers

PMID: 8287622
DOI: 10.1007/BF01784335

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Retinoic acid negatively regulates beta 4 integrin expression and suppresses the malignant phenotype in a Lewis lung carcinoma cell line.PMID 8287622Read ↗

Tumor-suppressive effect of the retinoic acid receptor beta in human epidermoid lung cancer cells.Semantic proximity Read ↗

All-trans-retinoic acid alters myc gene expression and inhibits in vitro progression in small cell lung cancer.Semantic proximity Read ↗

Effects of retinoic acid on cell differentiation and reversion toward normal in human endometrial adenocarcinoma (RL95-2) cells.Semantic proximity Read ↗

Quantitative switch in integrin expression accompanies differentiation of F9 cells treated with retinoic acid.Semantic proximity Read ↗

Increased retinoic acid responsiveness in lung carcinoma cells that are nonresponsive despite the presence of endogenous retinoic acid receptor (RAR) beta by expression of exogenous retinoid receptors retinoid X receptor alpha, RAR alpha, and RAR gamma.Semantic proximity Read ↗

Cell adhesion-mediated transformation of a human SCLC cell line is associated with the development of a normal phenotype.Semantic proximity Read ↗

Retinoid receptors in human lung cancer and breast cancer.Semantic proximity Read ↗

Evidence for impaired retinoic acid receptor-thyroid hormone receptor AF-2 cofactor activity in human lung cancer.Semantic proximity Read ↗

Retinoic acid fails to induce expression of Hox genes in differentiation-defective murine embryonal carcinoma cells carrying a mutant gene for alpha retinoic acid receptor.Semantic proximity Read ↗

Suppression of proliferation, tumorigenicity and metastasis of lung cancer cells after their transduction by interferon-beta gene in baculovirus vector.Semantic proximity Read ↗

Modulators of intracellular Ca2+ and the calmodulin inhibitor W-7 alter the expression of metastasis-associated genes MTS1 and NM23 in metastatic variants of the B16 murine melanoma.Semantic proximity Read ↗

Retinoic acid-induced differentiation of a nontumorigenic embryonal carcinoma cell mutant created through retroviral insertion.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.