DAOLUN YU¹, DEYONG SHE², KAI GE¹, LEI YANG¹, RUINA ZHAN¹, SHAN LU^3,*, YAFEI CAI^4,*

BIOCELL, Vol.48, No.1, pp. 139-147, 2024, DOI:10.32604/biocell.2023.045884 - 30 January 2024

Abstract Background: SMAD family proteins (SMADs) are crucial transcription factors downstream of transforming growth factor beta (TGF-ß)/SMAD signaling pathways that have been reported to play a pivotal role in mammalian reproduction. However, the role of SMAD family member 8 (SMAD8, also known as SMAD9), a member of the SMAD family, in mammalian reproduction remains unclear. Methods: We employed RNA interference techniques to knock down Smad8 expression in mouse granulosa cells (GCs) to investigate the effects of Smad8 on GC growth and steroidogenesis. Results: Our findings revealed a significant decrease in the proliferative capacity and a substantial increase in… More >

Jianping Xu, Liguo Sun, Wei Sun, Jianhai Tian, Huaiyuan Guo

Oncology Research, Vol.26, No.7, pp. 997-1003, 2018, DOI:10.3727/096504017X15140544654946

Abstract To investigate the effect of Kim-1 on 786-0 cells in vivo and in vitro, several experiments such as quantitative real-time PCR, Western blot, MTT, colony formation, and flow cytometry were performed to evaluate the biological behavior of 786-0 cells treated with Kim-1 siRNA. Furthermore, the tumor xenograft model was applied to BALB/c nude mice to assess the effect of Kim-1 silencing. Lentivirus-mediated RNAi effectively silenced Kim-1 in 786-0 cells. Kim-1 knockdown significantly inhibited the proliferation and colony formation ability of 786-0 cells (p < 0.01). The cell cycle of 786-0 cells was arrested in the G₀/G₁ phase (p < More >

Jianpeng Liu^*, Wei Li^†, Shunshun Liu^*, Xu Zheng^*, Lin Shi^*, Weitao Zhang^*, Hongfa Yang^*

Oncology Research, Vol.25, No.2, pp. 225-232, 2017, DOI:10.3727/096504016X14732772150587

Abstract Collagen triple helix repeat containing 1 (CTHRC1), an extracellular matrix-related protein, has been found to be upregulated in many solid tumors and contributes to tumorigenesis. We found that CTHRC1 is overexpressed in glioblastoma tissues and cells. By using the technique of RNA interference, the expression of CTHRC1 in the human glioblastoma U-87MG cell line was downregulated, and the proliferation and migration of U-87MG cells were examined. The results showed that the knockdown of CTHRC1 exerts inhibitory effects on the proliferation and migration ability of U-87MG cells. Knockdown of CTHRC1 expression in U-87MG cells resulted in More >

Gaowu Hu^*, Ye Xu^*, Wenquan Chen^*, Jiandong Wang^†, Chunying Zhao^†1, Ming Wang^*1

Oncology Research, Vol.24, No.6, pp. 455-461, 2016, DOI:10.3727/096504016X14685034103635

Abstract Breast cancer is a highly prevalent disease affecting women. The association of IQ motif containing GTPaseactivating protein 3 (IQGAP3) and breast cancer is poorly defined. Here we reported that IQGAP3 is a key regulator of cell proliferation and metastasis during breast cancer progression. The expression of IQGAP3 was significantly increased in breast tissues compared to nontumor tissues at both protein and mRNA levels. Furthermore, IQGAP3 had a high expression level in ZR-75-30 and BT474 compared to other breast cancer cell lines. Depletion of IQGAP3 through RNA interference in ZR-75-30 and BT474 significantly inhibited cell proliferation. More >

Qian Li, Jing Jin, Jianghui Liu, Liqun Wang, Yutong He

Oncology Research, Vol.24, No.3, pp. 205-214, 2016, DOI:10.3727/096504016X14648701447896

Abstract We recently found that SLC39A5 (ZIP5), a zinc transporter, is overexpressed in esophageal cancer. Downregulation of ZIP5 inhibited the proliferation, migration, and invasion of the esophageal cancer cell line KYSE170 in vitro. In this study, we found that downregulation of SLC39A5 (ZIP5) by interference resulted in a significant reduction in esophageal cancer tumor volume and weight in vivo. COX2 (cyclooxygenase 2) expression was decreased and E-cadherin expression was increased in the KYSE170K xenografts, which was caused by the downregulation of ZIP5. However, we did not find that the downregulation of ZIP5 caused a change in More >