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  • Open Access

    ARTICLE

    ROR2 promotes invasion and chemoresistance of triple-negative breast cancer cells by activating PI3K/AKT/mTOR signaling

    XIA DA1, HAN GE2, JUNFENG SHI3, CHUNHUA ZHU1, GUOZHU WANG1, YUAN FANG4,*, JIN XU1,*

    Oncology Research, Vol.32, No.7, pp. 1209-1219, 2024, DOI:10.32604/or.2024.045433

    Abstract Objective: This study aimed to investigate the role of receptor tyrosine kinase-like orphan receptor 2 (ROR2) in triple-negative breast cancer (TNBC). Methods: ROR2 expression in primary TNBC and metastatic TNBC tissues was analyzed by immunohistochemical staining and PCR. ROR2 expression in TNBC cell lines was detected by PCR and Western blot analysis. The migration, invasion and chemosensitivity of TNBC cells with overexpression or knockdown of ROR2 were examined. Results: ROR2 expression was high in metastatic TNBC tissues. ROR2 knockdown suppressed the migration, invasion and chemoresistance of TNBC cells. ROR2 overexpression in MDA-MB-435 cells promoted the migration, More >

  • Open Access

    ARTICLE

    OPA3 overexpression modulates lipid droplet production and sensitizes colorectal cancer cells to bevacizumab treatment

    HONGBIAO WU*, DONGFANG LIU

    BIOCELL, Vol.48, No.6, pp. 971-980, 2024, DOI:10.32604/biocell.2024.049466

    Abstract Background: Colorectal cancer (CRC) represents a substantial risk to public health. Bevacizumab, the first US FDA-approved antiangiogenic drug (AAD) for human CRC treatment, faces resistance in patients. The role of lipid metabolism, particularly through OPA3-regulated lipid droplet production, in overcoming this resistance is under investigation. Methods: The protein expression pattern of OPA3 in CRC primary/normal tissues was evaluated by bioinformatics analysis. OPA3-overexpressed SW-480 and HCT-116 cell lines were established, and bevacizumab resistance and OPA3 effects on cell malignancy were examined. OPA3 protein/mRNA expression and lipid droplet-related genes were measured with Western blot and qRT-PCR. OPA3… More > Graphic Abstract

    OPA3 overexpression modulates lipid droplet production and sensitizes colorectal cancer cells to bevacizumab treatment

  • Open Access

    ARTICLE

    UBE2T mediates the stemness properties of breast cancer cells through the mTOR signaling pathway

    JIAWEI YIN1, YONGSHENG WANG2,3, GUANGWEI WEI4, MINGXIN WEN3,*

    BIOCELL, Vol.48, No.6, pp. 959-970, 2024, DOI:10.32604/biocell.2024.049349

    Abstract Objectives: This study aimed to reveal the role and possible mechanism of the ubiquitin-conjugating enzyme 2T (UBE2T) in the biological activities of breast cancer stem cells (BCSCs). Methods: The specific protein and gene expression were quantified by Western blotting and quantitative real-time polymerase chain reaction, the proportion of BCSCs was examined by flow cytometry, and the self-renewal and proliferation of BCSCs were verified by serial sphere formation and soft agar. Results: Increasing expression of UBE2T was drastically found in breast cancer than that in adjacent tissues. Furthermore, UBE2T overexpression significantly increased the proportion of BCSCs in More >

  • Open Access

    ARTICLE

    Knockdown of SPOCK1 Inhibits the Proliferation and Invasion in Colorectal Cancer Cells by Suppressing the PI3K/Akt Pathway

    Ping Zhao*, Hai-Tao Guan, Zhi-Jun Dai, Yu-Guang Ma, Xiao-Xu Liu, Xi-Jing Wang

    Oncology Research, Vol.24, No.6, pp. 437-445, 2016, DOI:10.3727/096504016X14685034103554

    Abstract Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan (testican) 1 (SPOCK1), known as testican-1, were found to be involved in the development and progression of tumors. However, in colorectal cancer (CRC), the expression pattern of SPOCK1 and its functional role remain poorly investigated. In the present study, we explored the role of SPOCK1 in CRC. Our results demonstrated that SPOCK1 is overexpressed in CRC cell lines. SPOCK1 silencing significantly inhibited the proliferation in vitro and the tumor growth in vivo. Furthermore, SPOCK1 silencing significantly attenuated the migration/invasion by reversing the EMT process in CRC cells. Finally, knockdown More >

  • Open Access

    ARTICLE

    miR-489 Suppresses Proliferation and Invasion of Human Bladder Cancer Cells

    Jing Li, Weixing Qu, Yazhou Jiang, Yi Sun, Yongyi Cheng, Tiejun Zou, Shuangkuan Du

    Oncology Research, Vol.24, No.6, pp. 391-398, 2016, DOI:10.3727/096504016X14666990347518

    Abstract MicroRNAs (miRNAs) have been shown to be involved in bladder cancer progression. miR-489 (also known as miR-489-3p) was recently reported to be a tumor suppressor in several cancers. However, its exact role and mechanism in the progression of bladder cancer are largely unknown. In this study, we explore the role of miR-489 in the proliferation and invasion of human bladder cancer cells. The miR-489 expression levels were detected in bladder cancer and normal adjacent tissues, as well as in human normal bladder epithelial cells and bladder cancer cell lines. The results showed that miR-489… More >

  • Open Access

    ARTICLE

    Knockdown of Long Noncoding RNA uc.338 by siRNA Inhibits Cellular Migration and Invasion in Human Lung Cancer Cells

    Xuexin Gao*, Xuezhen Gao, Chao Li*, Yukun Zhang*, Lei Gao

    Oncology Research, Vol.24, No.5, pp. 337-343, 2016, DOI:10.3727/096504016X14666990347671

    Abstract Lung cancer remains a critical health concern worldwide. Long noncoding RNAs with ultraconserved elements have recently been implicated in human tumorigenesis. The present study investigated the role of ultraconserved element 338 (uc.338) in the regulation of cell proliferation and metastasis in human lung cancer. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Depletion of uc.338 with specific siRNA interference retarded the cell proliferative rate in lung cancer cell lines NCI-H929 and H1688. Furthermore, knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in More >

  • Open Access

    ARTICLE

    Ritonavir Interacts With Belinostat to Cause Endoplasmic Reticulum Stress and Histone Acetylation in Renal Cancer Cells

    Makoto Isono, Akinori Sato, Kazuki Okubo, Takako Asano, Tomohiko Asano

    Oncology Research, Vol.24, No.5, pp. 327-335, 2016, DOI:10.3727/096504016X14666990347635

    Abstract The histone deacetylase (HDAC) inhibitor belinostat increases the amount of unfolded proteins in cells by promoting the acetylation of heat shock protein 90 (HSP90), thereby disrupting its chaperone function. The human immunodeficiency virus protease inhibitor ritonavir, on the other hand, not only increases unfolded proteins by suppressing HSP90 but also acts as a proteasome inhibitor. We thought that belinostat and ritonavir together would induce endoplasmic reticulum (ER) stress and kill renal cancer cells effectively. The combination of belinostat and ritonavir induced drastic apoptosis and inhibited the growth of renal cancer cells synergistically. Mechanistically, the combination More >

  • Open Access

    ARTICLE

    TIPE2 Overexpression Suppresses the Proliferation, Migration, and Invasion in Prostate Cancer Cells by Inhibiting PI3K/Akt Signaling Pathway

    Qiang Lu, Zhe Liu, Zhuo Li, Jia Chen, Zhi Liao, Wan-rui Wu, Yuan-wei Li

    Oncology Research, Vol.24, No.5, pp. 305-313, 2016, DOI:10.3727/096504016X14666990347437

    Abstract Tumor necrosis factor-a (TNF-a)-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is involved in the invasion and metastasis of human tumors. However, the functional role of TIPE2 in prostate cancer remains unclear. In the present study, we explored the role of TIPE2 in prostate cancer and cancer progression including the molecular mechanism that drives TIPE2-mediated oncogenesis. Our results showed that TIPE2 was lowly expressed in human prostate cancer tissues and cell lines. In addition, restored TIPE2 obviously inhibits proliferation in prostate cancer cells. TIPE2 overexpression also suppresses the epithelial–mesenchymal transition (EMT) process and migration/invasion in prostate cancer More >

  • Open Access

    ARTICLE

    Anexelekto (AXL) Increases Resistance to EGFR-TKI and Activation of AKT and ERK1/2 in Non-Small Cell Lung Cancer Cells

    Yaqiong Tian*1, Zengli Zhang†1, Liyun Miao*, Zhimin Yang, Jie Yang*, Yinhua Wang§, Danwen Qian, Hourong Cai*, Yongsheng Wang*

    Oncology Research, Vol.24, No.5, pp. 295-303, 2016, DOI:10.3727/096504016X14648701447814

    Abstract Recently, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have revolutionized nonsmall cell lung cancer (NSCLC) treatment. However, resistance remains a major obstacle. Anexelekto (AXL) is a member of receptor tyrosine kinases (RTKs) and shares the same downstream signaling pathways with EGFR, such as PI3K/AKT and MAPK/ERK. AXL overexpression in resistant tumors has been implicated in many previous studies in vitro and in vivo. In this study, we further examined whether expression of AXL and its downstream targets increased in gefitinib-resistant PC9 cells (PC9GR). In addition, we hypothesize that knocking down AXL in PC9GR and… More >

  • Open Access

    ARTICLE

    Knockdown of Rap1b Enhances Apoptosis and Autophagy in Gastric Cancer Cells via the PI3K/Akt/mTOR Pathway

    Yazhou Li*†, Yang Liu, Feiyu Shi, Liang Cheng, Junjun She

    Oncology Research, Vol.24, No.5, pp. 287-293, 2016, DOI:10.3727/096504016X14648701447779

    Abstract Gastric cancer (GC) is the fourth most common malignancy and the second leading cause of cancer mortality around the world. However, the regulatory mechanisms of GC tumorigenesis and cancer cell motility are completely unknown. We investigated the role of a RAS-related protein (Rap1b) in the progression of GC. Our results showed that the expression of Rap1b is aberrantly upregulated in GC tissue samples and human GC cell lines, and the high expression of Rap1b indicated a positive correlation with poor prognosis in patients with GC. Inhibition of endogenous Rap1b dramatically reduced the cell cycle progression… More >

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