Interleukin-6 (IL-6) Functions as an Autocrine Growth Factor in Cervical Carcinomas in Vitro

Interleukin-6 promotes cervical tumor growth by VEGF-dependent angiogenesis via a STAT3 pathway

“…This study transfected IL-6 gene into an IL-6 null cervical cancer cell line C33A and confirmed that IL-6 expression promotes cervical tumor growth in nude mice. Although previous studies showed that IL-6 could promote the growth of both normal and neoplastic cervical epithelial cells (Eustace et al, 1993;Castrilli et al, 1997), IL-6 appeared to play a limited role in the proliferation of C33A cervical cancer cells because all the parental, neo control, and IL-6-overexpressed C33A cells displayed similar in vitro growth kinetics ( Figure 1a, b). Our experimental results provide evidence that IL-6 promotes cervical tumorigenesis by activating Figure 4 Effects of anti-VEGF treatment on C33A/IL-6 xenograft in nude mice.…”

Transforming growth factor-β1 activates interleukin-6 expression in prostate cancer cells through the synergistic collaboration of the Smad2, p38-NF-κB, JNK, and Ras signaling pathways

“…In addition, IL-6 has been implicated in the pathology of a variety of malignant tumors including myeloma, renal cell carcinoma, and cervical carcinoma (Miki et al, 1989;Akira and Kishimoto, 1992;Eustace et al, 1993). IL-6 expression is upregulated in several solid and hematopoietic neoplasms and elevated levels of circulating IL-6 have been reported to be associated with poor outcome of the diseases (Miki et al, 1989;Akira and Kishimoto, 1992;Eustace et al, 1993;Oka et al, 1996;Seymour et al, 1997) Autocrine growth stimulation and/or apoptosis inhibition via phosphoinositide-3-kinase (PI3K) activation have been suggested as the possible mechanisms for the oncogenic action of IL-6 (Miki et al, 1989;Akira and Kishimoto, 1992;Eustace et al, 1993). In the prostate, high levels of IL-6 secretion were found in the sera of patients with metastatic prostate carcinoma, and increased serum IL-6 levels correlate with hormone-refractory disease and cancer morbidity (Twillie et al, 1995;Adler et al, 1999;Drachenberg et al, 1999).…”

Interleukin-6 dependent induction of the cyclin dependent kinase inhibitor p21WAF1/CIP1 is lost during progression of human malignant melanoma

“…Other biological roles IL-6 is known to play include immunological and in¯ammatory reactions, cell di erentiation, angiogenesis and acute phase responses (Kishimoto et al, 1995;Kishimoto, 1989). Many of these activities involve autocrine or paracrine regulation of cell growth (Okamoto et al, 1997;Chiu et al, 1996;Eustace et al, 1993;Miki et al, 1989;Zhang et al, 1989;Kawano et al, 1988), motility (Swope et al, 1991) or apoptosis (Mizutani et al, 1995;Borsellino et al, 1995).…”