Gene expression analyses associated with malignant phenotypes of metastatic sub-clones derived from a mouse oral squamous cell carcinoma Sq-1979 cell line

Abstract

Abstract. To elucidate the genetic events that occur during the development of OSCC, the present study established a model of oral malignancy using a mouse oral squamous cell carcinoma (OSCC) Sq-1979 cell line. Sq-1979 cells were implanted into syngeneic C3H mice. Subsequently, 233 cells and metastatic sub-clones (L cells) from primary OSCC, as well as the metastasized lymph node tissues of Sq-1979-implanted mice were established. Compared with parental Sq-1979 and 233 cells, the majority of L cells exhibited a higher proliferation rate and transplantability, and conferred a lower survival rate on the implanted mice. To investigate the genetic background of L cells, preferentially expressed genes in L cells were identified by cDNA microarray and reverse transcription-polymerase chain reaction analyses. The expression of FYN-binding protein (Fyb), solute carrier family 16 member 13 (Slc16a13), keratin 7, transmembrane portion 173 and Slc44a3 mRNAs was significantly elevated in L cells compared with that in Sq1979 and 233 cells. The mRNA expression was also evaluated in human OSCC and leukoplakia (LP) tissues. Among the 5 aforementioned mRNAs, the expression of FYB and SLC16A13 was significantly higher in OSCC than in LP tissues. Furthermore, the expression of SLC16A13 mRNA was significantly elevated in highly invasive OSCCs, which were classified as grades 3 and 4 by the Yamamoto-Kohama (YK) classification of invasion, compared with those in lower grades (YK-1 and -2). The model proposed in the present study could thus describe essential marker genes for the diagnosis of oral malignancies.

Development of a prognostic model for glioblastoma multiforme based on the expression levels of efferocytosis-related genes

“…Recent research demonstrated that the solute carrier (SLC) family of membrane transport proteins plays a role in modulating efferocytosis by upregulating the expression levels of anti-inflammatory genes and sustaining continuous efferocytosis [ 37 ]. It was reported that SLC16A13 could be a potential biomarker for tumor prognosis, including oral squamous cell carcinoma, lung adenocarcinoma, and pancreatic cancer [ 38 – 40 ]. However, the relationship between these two genes and GBM has not yet been explored.…”

Mouse Models for Immune Checkpoint Blockade Therapeutic Research in Oral Cancer

“…The principle of syngeneic models is similar to the cell-derived xenograft (CDX) model. Several mouse cell lines can be used to develop syngeneic OSCC mouse models, including mouse OSCC Sq-1979 cells [ 36 ], mouse squamous cell carcinoma SCC7 [ 37 , 38 ], mouse oral cancer (MOC) cell lines [ 40 ], MOC1 [ 41 ], and MOC2 [ 42 ]. Moroishi et al [ 39 ] have demonstrated that transplanting SCC7 cells (1 × 10 5 ) into both hind flanks of C3H/HeOu mice resulted in aggressive tumor growth, whereas LATS1/2 dKO SCC7 cells did not result in tumors.…”

“…Nagaya et al [ 40 ] studied the effects of near-infrared photoimmunotherapy using syngeneic models developed through the subcutaneous injection of C57BL/6 mice with poorly immunogenic MOC2 mKate2 cells (1.5 × 10 5 ), moderately immunogenic MOC2-luc cells (1.5 × 10 5 ), and immunogenic MOC1 cells (2.0 × 10 6 ). Similarly, Adachi et al [ 36 ] injected Sq-1979 cells (1 × 10 7 ) into the posterior neck area of C3H/HeN mice to determine the genetic changes that occur throughout OSCC development. These studies demonstrate that different mouse OSCC cell lines could be successfully used to produce stable syngeneic OSCC models.…”

Perspectives of Immune Suppression in the Tumor Microenvironment Promoting Oral Malignancy

“…In order to compare the immune-modulatory effects of OSCCs in primary and advanced stages, we have established a metastasized model (L5-11cells) representing more malignant phenotypes than the parental OSCC (Sq-1979 cells) when implanted in the syngeneic mice [ 82 ]. Our results revealed that it is metastasized L5-11 cells, not early-stage Sq-1979 cells that predominantly induce PMN-MDSCs in tumor-bearing mice [ 83 ]; this is not simply reflecting the differential tumor size, since even the larger amount of inoculation of Sq1979 cells could not induce the MDSC cells in the mice.…”