4.2 Article

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

Journal

ACTA HISTOCHEMICA
Volume 123, Issue 1, Pages -

Publisher

ELSEVIER GMBH
DOI: 10.1016/j.acthis.2020.151657

Keywords

Hodgkin's lymphoma; Reed-Sternberg; Prolactin receptor; Cancer; Immunohistochemistry

Categories

Funding

  1. PSC-CUNY Award - Professional Staff Congress
  2. PSC-CUNY Award - City University of New York [TRADB-48-360]
  3. City University of New York Community College Research Grant [80212-03-17]

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The study showed that Prolactin receptor (PRLR) is overexpressed in Hodgkin's lymphoma and may play a role in tumor growth. However, further research is needed to understand the precise role of PRLR in the pathogenesis of Hodgkin's lymphoma.
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 5-mu m 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 mu M 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 siRNA-depletion 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.

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