Immunohistochemical localization of prolactin receptor (PRLR) to Hodgkin’s and Reed-Sternberg cells of Hodgkin’s lymphoma

Abstract

Prolactin receptor (PRLR), a type-1 cytokine receptor, is overexpressed in a number of cancer types. It has attracted much attention for putative pro-oncogenic roles, which however, remains controversial in some malignancies. In this study, we reported the localization of PRLR to the Hodgkin's and Reed-Sternberg (HRS) cells of Hodgkin's lymphoma (HL), a neoplasm of predominantly B cell origin. Immunohistochemistry performed on 5μm thick FFPE sections revealed expression of PRLR in HRS cells. Cellular immunofluorescence experiments showed that the HL-derived cell lines, Hs445, KMH2 and L428 overexpressed PRLR. The PRLR immunofluorescent signal was depleted after treating the cell lines with 10 μM of siRNA for 48 h. We also tested whether PRLR is involved in the growth of HL, in vitro. One-way analysis of variance (ANOVA) on cell growth data obtain from WST-1 cell proliferation assay and trypan blue exclusion assay and hemocytometry showed that siRNAdepletion of PRLR expression resulted in decreased growth in all three cell lines. These results offered only a short insight into the involvement of PRLR in HL. As a result, further investigation is required to decipher the precise role(s) of PRLR in the pathogenesis of HL.

PRLR and CACNA2D1 Impact the Prognosis of Breast Cancer by Regulating Tumor Immunity

“…PRLR is the receptor of prolactin that promotes the growth of breast tissues, and it belongs to the transmembrane receptor of cytokine receptor family [22]. Previous studies have found that PRLR plays an important role in pancreatic cancer [23], ovarian cancer [24], prostate cancer [25], Hodgkin's lymphoma [26], prolactinoma [27], and BC [28]. PRLR is expressed in most BC cells, but no consensus has been reached regarding whether it is overexpressed in BC tissues.…”

Piperlongumine inhibits proliferation and oncogenic MYCN expression in chemoresistant metastatic retinoblastoma cells directly and through extracellular vesicles

“…RNA isolation, cDNA synthesis, and qPCR were performed as described by Gharbaran et al [ 38 ], using Y79 cells treated with 10 μM PL and their EVs and untreated control Y79 cells and their EVs. Total RNA was isolated by Trizol (Life Technologies, Carlsbad; CA, USA, cat.…”

Diminazene aceturate‐induced cytotoxicity is associated with the deregulation of cell cycle signaling and downregulation of oncogenes Furin, c‐MYC, and FOXM1 in human cervical carcinoma Hela cells

“…Cellular immunofluorescence was carried out as described by Gharbaran et al [27,[29][30][31] with modifications. Hela cells grown on chamber slides were fixed for 10 min with 4% paraformaldehyde (Electron Microscopy Sciences 15710) and then permeabilized with 0.1% PBS-Triton X-100 (Sigma-Aldrich) for 10 min.…”