Biochemical and Biophysical Research Communications
Regular ArticleCancer Cells Responsible for Humoral Hypercalcemia Express mRNA Encoding a Secreted Form of ODF/TRANCE That Induces Osteoclast Formation☆
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Parathyroid hormone-related protein (PTHrP) and malignancy
2022, Vitamins and HormonesCitation Excerpt :PTHrP is produced and released by a variety of tumors, including squamous cell carcinomas such as lung, head and neck, renal, bladder, ovarian and breast cancers. In addition to PTHrP, a number of other circulating proinflammatory cytokines (including EGF, GCSF, TNF-alpha, IL-1, IL-5, IL-6, IL-8 and IL-11) have been implicated in HHM to a more limited degree (Horwitz & Stewart, 2003; Nagai, Kyakumoto, & Sato, 2000). While HHM is typically a late finding in advanced metastatic disease associated with a poor and short-term prognosis (Bhandari et al., 2019), breast cancer patients experience a somewhat longer median survival of 3–4.5 months (de Wit & Cleton, 1994).
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2013, Taiwanese Journal of Obstetrics and GynecologyCitation Excerpt :It is possible that most of the participants were in the early postmenopausal stage in which trabecular bone (the main component of lumbar spine) loss was more prevalent [26]. The RANKL gene encodes two different mRNAs and thus two different proteins of 244 (variant 1) [27] and 317 (variant 2) [28] amino acids. Variant 2 has 73 more amino acids than variant 1 at the N-terminus.
RANKL synthesized by both stromal cells and cancer cells plays a crucial role in osteoclastic bone resorption induced by oral cancer
2013, American Journal of PathologyCitation Excerpt :We previously reported that RANKL synthesized by stromal cells plays an important role in osteoclastic bone resorption during oral cancer–associated bone destruction,7 as reported in cases of multiple myeloma,30 breast cancer,8–10 and prostate cancer.11,12 Production of RANKL by tumor cells has also been reported in multiple myeloma,17 breast cancer,9,14 renal cancer,16 prostate cancer,15 and oral cancers.18–20 Although these results suggest that RANKL produced by tumor cells is also involved in cancer-associated bone destruction, it has not been demonstrated that the RANKL produced by tumor cells actually participates in cancer-associated bone resorption.
Oral squamous carcinoma cells secrete RANKL directly supporting osteolytic bone loss
2013, Oral OncologyCitation Excerpt :Recent studies suggest OSCC cells are capable of regulating osteoclastogenesis as well as mature osteoclast function through numerous mechanisms, including RANKL/OPG signaling.22 In vitro studies have demonstrated in multiple myeloma as well as two oral squamous cell carcinoma cell lines, the ability of cancer cells to produce RANKL and induce osteoclastogenesis.23,24 As an essential factor for osteoclastogenesis, RANKL expression can be induced in stromal cells, including osteoblasts, by a variety of hormonal and cytokine stimuli including vitamin D3,25 IL-1β, IL-6, PTHrP, and IL-17.26
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Abbreviations used: ODF, osteoclast differentiation factor; TRANCE, tumor necrosis factor-related activation-induced cytokine; sODF/TRANCE, soluble fragment of ODF/TRANCE; ORF, open reading frame; OCL(s), osteoclast like cell(s); TNF, tumor necrosis factor; OPGL, osteoprotegerin ligand; RANKL, receptor activator of NF-kB ligand; HHM, humoral hypercalcemia of malignancy; PTHrP, parathyroid hormone-related protein; FBS, fetal bovine serum; RACE, rapid amplification of cDNA ends; Ab, antibody; CT-R, calcitonin receptor; RANK, receptor activator of NF-κB; nt, nucleotide
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