Podocalyxin is crucial for the growth of oral squamous cell carcinoma cell line HSC-2

Abstract

Oral cancers constitute approximately 2% of all cancers, with the most common histological type being oral squamous cell carcinoma (OSCC), representing 90% of oral cancers. Although diagnostic technologies and therapeutic techniques have progressed, the survival rate of patients with OSCC is still 60%, whereas the incidence rate has increased. Podocalyxin (PODXL) is a highly glycosylated type I transmembrane protein that is detected in normal tissues such as heart, breast, and pancreas as well as in many cancers, including lung, renal, breast, colorectal, and oral cancers. This glycoprotein is associated with the progression, metastasis, and poor outcomes of oral cancers. PODXL overexpression was strongly detected using our previously established anti-PODXL monoclonal antibody (mAb), PcMab-47, and its mouse IgG2a-type, 47-mG2a. In previous studies, we also generated PODXL-knock out (PODXL-KO) cell lines using SAS OSCC cell lines, in order to investigate the function of PODXL in the proliferation of oral cancer cells. The growth of SAS/PODXL-KO cell lines was observed to be lower than that of parental SAS cells. For this study, PODXL-KO OSCC cell lines were generated using HSC-2 cells, and the role of PODXL in the growth of OSCC cell lines in vitro was assessed. Decreased growth was observed for HSC-2/PODXL-KO cells compared with HSC-2 parental cells. The influence of PODXL on tumor growth of OSCC was also investigated in vivo, and both the tumor volume and the tumor weight were observed to be significantly lower for HSC-2/PODXL-KO than that for HSC-2 parental cells. These results, taken together, indicate that PODXL plays an important role in tumor growth, both in vitro and in vivo.

Emerging Role of Podocalyxin in the Progression of Mature B-Cell Non-Hodgkin Lymphoma

“…In SAS human oral squamous cell carcinoma cell line, silencing of PODXL abrogated cell proliferation and colony formation [46]. This effect was corroborated in vivo by transplanting PODXL-silenced HSC-2 oral squamous cell carcinoma cell line into nude mice, which resulted in both tumor volume and tumor weight reduction compared to that derived from parental HSC-2 cells [79].…”

PODXL might be a new prognostic biomarker in various cancers: a meta-analysis and sequential verification with TCGA datasets

“…The clinical significance of PODXL in the progression of various cancers has been studied, and it was found as a stem cell marker in the testicular cancer at the first time [3]. The later findings proved that, PODXL associates with advanced tumor phenotype in some cancers, including breast cancer [1,13], colorectal cancer [5,[14][15][16], esophageal cancer [17], gastric cancer [17][18][19], glioblastoma multiforme [20], lung adenocarcinoma [21], oral squamous cell carcinoma [4,22], ovarian cancer [23], pancreatic cancer [24][25][26][27], prostate cancer [28,29], renal cell carcinoma [30], urothelial bladder cancer [31], and so on.…”

“…Podocalyxin-like protein (PODXL) is a highly glycosylated type I transmembrane protein associated with CD34 [2][3][4]. PODXL expression has been reported in the cytoplasm of some tumor cells, in some cases protruding toward the cell membrane, but not in the nucleus [5].…”

Radiation-Induced Overexpression of TGFβ and PODXL Contributes to Colorectal Cancer Cell Radioresistance through Enhanced Motility

“…PODXL is known to play a crucial role in maintaining adequate cellular infiltration because of its anti-adhesive properties; it can regulate cell adhesion by dissociating from actin, resulting in the loss of podocyte integrity [15][16][17]. PODXL has been reported to be overexpressed in a variety of malignancies, and strong cell-membrane expression has been associated with both tumor aggressiveness and poor prognoses in a variety of tumors, including CRC [18][19][20][21]. In addition, PODXL has been shown to act as an EMT mediator, to be involved in metastatic behavior, and to induce actin recruitment in several types of cancer cells [22][23][24].…”