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

Tao Xie^*, Yao Li^†, Shi-Lei Li^*, Hai-Feng Luo^‡

Oncology Research, Vol.24, No.6, pp. 447-453, 2016, DOI:10.3727/096504016X14685034103590

Abstract Although astragaloside IV exhibits anti-inflammation, immunoregulatory, and anticancer properties, the chemosensitization effects of astragaloside IV in colorectal cancer have never been reported. Our study tested whether astragaloside could increase cisplatin sensitivity in colorectal cancer. CCK-8 assay was used to measure the cell viability of colorectal cancer cells. Quantitative real-time PCR and Western blot were performed to determine the mRNA and protein expression, respectively. Our data revealed that astragaloside IV administration significantly suppressed the cell growth of colorectal cancer cells, whereas no obvious cytotoxicity of astragaloside IV was observed in nonmalignant colonic cells. In addition, combined… More >

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 >

Kazuyoshi Kawakami^*, Takashi Yokokawa^*, Kazuo Kobayashi^*, Takahito Sugisaki^*, Kenichi Suzuki^*, Mitsukuni Suenaga^†, Kensei Yamaguchi^†, Ayaka Inoue^‡, Yoshiaki Machida^‡, Toshiharu Yamaguchi^†, Toshihiro Hama^*

Oncology Research, Vol.25, No.9, pp. 1625-1631, 2017, DOI:10.3727/096504017X15012905098071

Abstract Adherence has become an important issue in modern oncology treatment. Most studies have included heterogeneous target tumor types, regimens, and therapy settings. Our study focused on capecitabine during capecitabine plus oxaliplatin (XELOX) treatment as an adjuvant therapy for colorectal cancer. The main aims of this study were to evaluate real-life adherence to capecitabine and to investigate candidate factors that might decrease adherence. We studied 338 consecutive patients who received XELOX treatment between December 1, 2011, and April 30, 2015, at the Cancer Institute Hospital of the Japanese Foundation for Cancer Research. Our study assessed adherence… More >

Hai-tao Geng^*, Rui-juan Cao^*, Lei Cheng^†, Chun-yuan Liu^†

Oncology Research, Vol.25, No.7, pp. 1039-1046, 2017, DOI:10.3727/096504016X14813914187138

Abstract Hepatocyte cell adhesion molecule (hepaCAM), a new type of CAM, belongs to the immunoglobulin superfamily. Recently, hepaCAM was reported to be implicated in cancer development, and many researchers investigated its biological function in the tumorigenesis of various cancers. However, what kind of role hepaCAM plays in colorectal cancer (CRC) remains unknown. In this study, we found that hepaCAM was downregulated in CRC tissues and cell lines. Overexpression of hepaCAM inhibited CRC cell proliferation, migration, and invasion in vitro. Furthermore, the tumorigenesis assay showed that increased expression of hepaCAM suppressed CRC tumor growth and metastasis in More >

Fen Liu^*†, Shaojun Liu^*, Feiyan Ai^*†, Decai Zhang^*†, Zhiming Xiao^*, Xinmin Nie^‡, Yunfeng Fu^§

Oncology Research, Vol.25, No.6, pp. 967-974, 2017, DOI:10.3727/096504016X14803476672380

Abstract Colorectal cancer (CRC) is one of the most common malignancies in the world, with a high incidence and a high mortality. However, the pathogenesis of CRC carcinogenesis is still unexplored. In this study, we investigated the role of miR-107 in the regulation of CRC cell proliferation and apoptosis. First, the expression of miR-107 was observed to be aberrantly increased in human CRC tumor tissues and cell lines when compared to the colonic control tissues and colon epithelial cells. Further study showed that the proliferative and apoptotic capacities of human CRC SW480 and LoVo cells were… More >

Feng Zhang^*, Hong Sun^†, Sai Zhang^†, Xin Yang^‡, Guogang Zhang^*, Tao Su^†

Oncology Research, Vol.25, No.5, pp. 709-719, 2017, DOI:10.3727/096504016X14772331883976

Abstract PER3, a circadian clock gene, plays an important role in colorectal cancer, but its action and underlying mechanism in colorectal cancer stem-like cells (CSCs) remain unclear. In this study, the colorectal CSCs were enriched in colorectal HCT-116 sphere-forming cells, expressing lower levels of stem cell markers CD133, CD44, LGR5, and SOX2 compared with HCT-116 cells. A drug-resistant strain from HCT-116 was established. Western blot and qRT-PCR analysis showed that PER3 was downregulated in colorectal CSCs and drug-resistant HCT-116. Overexpression of PER3 could strengthen 5-FU-induced inhibitory effects on colorectal CSCs, but knockdown of PER3 decreased its… More >

Sheng-Qiang Lu^*1, Yan Qiu^†1, Wei-Jie Dai^‡, Xiao-Yu Zhang^§

Oncology Research, Vol.25, No.5, pp. 681-689, 2017, DOI:10.3727/096504016X14771034190471

Abstract Forkhead box R2 (FOXR2), a member of the FOX gene family, has not been very well investigated for its role in cancer. A recent study has shown that FOXR2 is highly expressed in breast cancer samples and is associated with poor prognosis. In addition, FOXR2 was identified as an oncogene in medulloblastoma. Nevertheless, whether FOXR2 plays a role in colorectal cancer (CRC) remains unclear. In the present study, we conducted several in vitro and in vivo studies to investigate the expression and effect of FOXR2 in CRC. The study results demonstrated that FOXR2 was upregulated More >

Cheng-Jen Ma^*†‡, Ching-Wen Huang^*‡§, Yung-Sung Yeh^*†¶, Hsiang-Lin Tsai^*§#**, Huang-Ming Hu^††‡‡, I-Chen Wu^††‡‡, Tian-Lu Cheng^§§¶¶, Jaw-Yuan Wang^{*†‡§**¶¶}

Oncology Research, Vol.25, No.5, pp. 673-679, 2017, DOI:10.3727/97818823455816X14786040691928

Abstract We analyzed the results of previously treated patients with metastatic colorectal cancer (mCRC) who received regorafenib plus FOLFIRI with the irinotecan dose escalation on the basis of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) genotyping. Thirteen patients with previously treated mCRC were subjected to UGT1A1 genotyping between October 2013 and June 2015 and were administered regorafenib plus FOLFIRI with irinotecan dose escalation. Patients with UGT1A1*1/*1 and *1/*28 genotypes were administered 180 mg/m² of irinotecan, whereas those with the UGT1A1*28/*28 genotype were administered 120 mg/m2 of irinotecan. For all patients, the irinotecan dose was increased by 30 mg/m2 every… More >

Zhe Huang, Yong Feng

Oncology Research, Vol.25, No.5, pp. 651-661, 2017, DOI:10.3727/096504016X14752792816791

Abstract Cancer cell-derived exosomes have been actively released into the tumor microenvironment with pleiotropic roles in tumor growth and metastasis, including angiogenesis and immune modulation. However, the functions and underlying mechanisms of exosomes shed by colorectal cancer (CRC) cells under hypoxic conditions remain unknown. Here we found that exosomes derived from hypoxic CRC cells promoted the proliferation and migration of endothelial cells. Suppression of exosome secretion through RAB27a knockdown in CRC cells inhibited exosomal-induced proliferation and migration of endothelial cells. Furthermore, we discovered that these exosomes enriched with Wnt4 were dependent on HIF1α. Exosomal Wnt4 increased More >