YE ZHANG¹, YANAN LIANG², YAN WU², LIWEN SONG², ZUWANG ZHANG^2,*

Oncology Research, Vol.32, No.11, pp. 1747-1763, 2024, DOI:10.32604/or.2024.030945 - 16 October 2024

Abstract Background: Papillary thyroid cancer (PTC) is the most prevalent histological type of differentiated thyroid malignancy. Circular RNAs (circRNAs) have been implicated in the pathogenesis and progression of various cancers. circTIAM1 (hsa_circ_0061406) is a novel circRNA with aberrant expression in PTC. However, its functional roles in PTC progression remain to be investigated. Methods: The expression levels of circTIAM1 in the PTC and the matched para-cancerous tissues were detected by quantitative real-time reverse-transcription PCR (qRT-PCR). The subcellular localization of circTIAM1 was examined by fluorescence in-situ hybridization (FISH). Kaplan-Meier plot was used to analyze the association of clinicopathological features… More >

Gang Li^*, Tie Chong^*, Jie Yang^†, Hongliang Li^*, Haiwen Chen^*

Oncology Research, Vol.27, No.1, pp. 125-137, 2019, DOI:10.3727/096504018X15213115046567

Abstract KIFC1 (kinesin family member C1) plays a critical role in clustering of extra centrosomes in various cancer cells and thus could be considered as a promising therapeutic target. However, whether KIFC1 is involved in the procession of renal cell carcinoma (RCC) still remains unclear. In this study, we found that KIFC1 was upregulated in RCC tissues and is responsible for RCC tumorigenesis (p<0.001). The high expression of KIFC1 correlates with aggressive clinicopathologic parameters. Kaplan–Meier analysis suggested that KIFC1 was associated with poor survival prognosis in RCC. Silencing KIFC1 dramatically resulted in inhibition of proliferation, delayed the More >

Yang Cao^*, Xu Shi^†, Yingmin Liu^‡, Ren Xu^§, Qing Ai^*

Oncology Research, Vol.27, No.1, pp. 117-124, 2019, DOI:10.3727/096504018X15213031799835

Abstract MicroRNA-338-3p (miR-338-3p) has been reported to be a tumor suppressor in multiple cancer types. However, the biological role of miR-338-3p and its underlying mechanism in multiple myeloma (MM) remain unclear. In the present study, we investigated the biological role and potential of miR-338-3p in MM. We found that miR-338-3p was significantly decreased in newly diagnosed and relapsed MM tissues and cell lines. Overexpression of miR-338-3p in MM cells significantly inhibited proliferation and promoted apoptosis, caspase 3, and caspase 8 activity. Bioinformatics algorithm analysis predicted that cyclin-dependent kinase 4 (CDK4) was a direct target of miR-338-3p, More >