Chemoprevention of Low-Molecular-Weight Citrus Pectin (LCP) in Gastrointestinal Cancer Cells

Wang, Shi; Li, Pei; Lu, Shengmin; Ling, Zhi‐Qiang

doi:10.7150/ijbs.13988

Cited by 38 publications

(31 citation statements)

References 36 publications

(36 reference statements)

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“…Many types of pectin, especially the modified ones, have been associated with anti-cancer activity in both in vitro and in vivo studies, such as the reduction of cell proliferation, migration, adhesion, and the induction of apoptosis 6 – 10 . These anti-cancer activities were shown for modified pectins of citrus 11 – 14 , apple 15 , 16 , sugar beet 6 . and ginseng 8 .…”

Section: Introductionmentioning

confidence: 79%

Ripening-induced chemical modifications of papaya pectin inhibit cancer cell proliferation

Prado

Ferreira

Harazono

et al. 2017

Sci Rep

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Papaya (Carica papaya L.) is a fleshy fruit with a rapid pulp softening during ripening. Ripening events are accompanied by gradual depolymerization of pectic polysaccharides, including homogalacturonans, rhamnogalacturonans, arabinogalactans, and their modified forms. During intermediate phases of papaya ripening, partial depolymerization of pectin to small size with decreased branching had enhanced pectin anti-cancer properties. These properties were lost with continued decomposition at later phases of ripening. Pectin extracted from intermediate phases of papaya ripening markedly decreased cell viability, induced necroptosis, and delayed culture wound closing in three types of immortalized cancer cell lines. The possible explanation for these observations is that papaya pectins extracted from the third day after harvesting have disrupted interaction between cancer cells and the extracellular matrix proteins, enhancing cell detachment and promoting apoptosis/necroptosis. The anticancer activity of papaya pectin is dependent on the presence and the branch of arabinogalactan type II (AGII) structure. These are first reports of AGII in papaya pulp and the first reports of an in vitro biological activity of papaya pectins that were modified by natural action of ripening-induced pectinolytic enzymes. Identification of the specific pectin branching structures presents a biological route to enhancing anti-cancer properties in papaya and other climacteric fruits.

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Section: Introductionmentioning

confidence: 79%

Ripening-induced chemical modifications of papaya pectin inhibit cancer cell proliferation

Prado

Ferreira

Harazono

et al. 2017

Sci Rep

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“…Some studies have shown that silencing of cyclinB1 is usually accompanied by inhibition of EMT. [17][18][19] In the present study, we investigated the EMT-related markers; the results showed that knockdown of cyclinB1 reversed the progression of EMT and may affect the metastasis of HCC.…”

Section: Discussionmentioning

confidence: 94%

<p>Inhibition of cyclinB1 Suppressed the Proliferation, Invasion, and Epithelial Mesenchymal Transition of Hepatocellular Carcinoma Cells and Enhanced the Sensitivity to TRAIL-Induced Apoptosis</p>

Lv¹,

Ning²,

Li³

et al. 2020

OTT

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Background: CyclinB1 is highly expressed in various tumor tissues and plays an important role in tumor progression. However, its role in hepatocellular carcinoma (HCC) remains unclear. Therefore, the aim of this study was to explore the role of cyclinB1 in the development and progression of HCC. Methods: The expression of cyclinB1 was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) database, and detected in HCC tissues and HCC cell lines through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting. CyclinB1-short hairpin RNA (Sh-cyclinB1) was transfected into HCC cells to knockdown cyclinB1, and the effect of cyclinB1 knockdown on HCC was examined via the MTT assay, colony formation assay, wound healing assay, scratch assay, cell cycle analysis in vitro, and xenograft model in nude mice. In addition, the role of cyclinB1 on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis was measured using flow cytometry and Western blotting. Results: The GEPIA database analysis showed that cyclinB1 was highly expressed in HCC tissues. The results of qRT-PCR and Western blotting proved that the expression of cyclinB1 was significantly increased in HCC tissues and cell lines. The data of the MTT assay, colony formation assay, and cell cycle analysis indicated that cyclinB1 knockdown inhibited the proliferation of HCC cells. In addition, cell migration, invasion, and epithelial mesenchymal transition were also impaired by cyclinB1 knockdown. Furthermore, the xenograft model in nude mice demonstrated that inhibition of cyclinB1 suppressed tumor growth and metastasis in vivo. Finally, the results of flow cytometry and Western blotting indicated that inhibition of cyclinB1 enhanced the sensitivity of HCC cells to TRAIL-induced apoptosis. Conclusion: Overall, these data provide reasonable evidence that cyclinB1 may serve as a proto-oncogene during the progression of HCC.

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“…Similar results have been shown in early gastric cancer, mammary cancer, and melanoma where β-catenin has been found to be strongly associated with LN metastasis. [ 31 32 33 ] The interaction of VEGF receptors (VEGFRs) with the EMT pathways may explain this finding as VEGFR-1 activation has been shown to enhance translocation of β-catenin from its usual cell membrane-bound location to the cytoplasm and nucleus. [ 34 ]…”

Section: Discussionmentioning

confidence: 99%

The role of the endothelin axis in promoting epithelial to mesenchymal transition and lymph node metastasis in prostate adenocarcinoma

et al. 2017

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Introduction:Aberrant activation of endothelin (ET) axis has been identified as a key player in tumor growth and metastasis in several tumor types. However, little is known about the possible interaction of the ET with epithelial to mesenchymal transition (EMT), a process that transforms tumor cells in a motile, resistant to apoptosis phenotype prone to invasion and metastasis. The aim of this study was to investigate the activation of the ET axis in prostate adenocarcinoma and examine possible associations with EMT markers, lymph node (LN) metastasis, and other clinicopathological parameters.Materials and Methods:We immunohistochemically evaluated the expression of ET-1 and its receptors A and B (ET-A, ET-B) in 64 N0 and 23 N1 prostate adenocarcinoma cases. EMT markers E-cadherin, N-cadherin, and β-catenin and the transcriptional factor SNAIL were evaluated. We examined possible correlations of ET pathway members with EMT markers, LN status, Gleason grade, and T stage.Results:Our results revealed increased expression of ET-1 and ET-A (but not ET-B) in prostate carcinoma; both ET-1 and ET-A were associated with lymph metastasis and T stage but not with Gleason grade. We observed E-cadherin and β-catenin decrease/relocalization and increased N-cadherin expression. SNAIL also showed increased expression in tumor tissue and was associated with LN metastasis (Mann–Whitney test, P = 0.0032). Expression of ET-1 and ET-A correlated well with SNAIL expression (Spearman r, P = 0.0002 and P = 0.0176, respectively).Conclusions:These findings indicate that activation of the ET pathway may induce EMT through SNAIL activation and correlates with increased metastatic potential.

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Chemoprevention of Low-Molecular-Weight Citrus Pectin (LCP) in Gastrointestinal Cancer Cells

Cited by 38 publications

References 36 publications

Ripening-induced chemical modifications of papaya pectin inhibit cancer cell proliferation

Ripening-induced chemical modifications of papaya pectin inhibit cancer cell proliferation

<p>Inhibition of cyclinB1 Suppressed the Proliferation, Invasion, and Epithelial Mesenchymal Transition of Hepatocellular Carcinoma Cells and Enhanced the Sensitivity to TRAIL-Induced Apoptosis</p>

The role of the endothelin axis in promoting epithelial to mesenchymal transition and lymph node metastasis in prostate adenocarcinoma

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