NIH3T3 cells overexpressing CD98 heavy chain resist early G1 arrest and apoptosis induced by serum starvation

Kaori Hara, Shiho Ueda, Yoshiya Ohno, Toshiyuki Tanaka, Hideki Yagi, Shogo Okazaki, Rieko Kawahara, Takechi Masayuki, Takemi Enomoto, Yoshiyuki Hashimoto, Kazue Masuko, Takashi Masuko

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


CD98 is a heterodimeric glycoprotein of 125-kDa, which consists of a 90-kDa heavy chain (hc) subunit and 35-kDa to 55-kDa light chain (lc) subunits. It is strongly expressed on the surface of proliferating normal cells and almost all tumor cells. To investigate the participation of CD98 in cellular proliferation and malignant transformation, we analyzed cell-cycle progression of NIH3T3 clones transfected with cDNA of human CD98hc. Although NIH3T3 and control transfectant cells grown to the subconfluent state were arrested in the G0/G1 phase by serum starvation, considerable portions of CD98hc-transfected cells resided at S and G2/M phases. Under serum-starved and confluent conditions, significant fractions (20-25%) of NIH3T3 and control transfectant cells contained less than 2n content DNA, indicating occurrence of apoptosis, whereas no apoptotic cells were detected in CD98hc-transfectant cells. Under serum-starved conditions, a marked increase in the levels of cyclin D1 and cyclin E and a decrease in p16 were observed in CD98hc-transfectant cells. The reverse was true for NIH3T3 and control transfectant cells. Our results suggest that resistance to G1 arrest and apoptosis by CD98 overexpression are associated with high G1-cyclins and low p16 levels.

Original languageEnglish
Pages (from-to)1460-1466
Number of pages7
JournalCancer Science
Issue number8
Publication statusPublished - Aug 2012
Externally publishedYes


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