Effect of Spirogyra neglecta on the early stages of 1, 2-dimethylhydrazine-induced colon carcinogenesis in rats

Taya, Sirinya; Thumvijit, Tarika; Chewonarin, Teera; Punvittayagul, Charatda; Wongpoomchai, Rawiwan

doi:10.1097/cej.0000000000000320

Cited by 2 publications

(3 citation statements)

References 40 publications

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“…During colorectal cancer progression, survivin obviously has the dual function of preventing tumor cell apoptosis and controlling the cell-cycle proliferation. This peculiarity concurs to both accelerate proliferative activity and suppress apoptosis [27-28]. High survivin expression has been observed in various types of tumors and therefore may represent a promising drug target for tumor treatment [29].…”

Section: Discussionmentioning

confidence: 99%

Bone Marrow Cell Therapy on 1,2-Dimethylhydrazine (DMH)-Induced Colon Cancer in Rats

El‐Khadragy

Nabil

Hassan

et al. 2018

Cell Physiol Biochem

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Background/Aims: Stem cell based therapies are being under focus due to their possible role in treatment of various tumors. Bone marrow stem cells believed to have anticancer potential and are preferred for their activities by stimulating the immune system, migration to the site of tumor and ability for inducting apoptosis in cancer cells. The current study was aimed to investigate the tumor suppressive effects of bone marrow cells (BMCs) in 1,2-dimethylhydrazine (DMH)-induced colon cancer in rats. Methods: The rats were randomly allocated into four groups: control, BMCs alone, DMH alone and BMCs with DMH. BMCs were injected intrarectally while DMH was injected subcutaneously at 20 mg/kg body weight once a week for 15 weeks. Histopathological examination and gene expression of survivin, β-catenin and multidrug resistance-1 (MDR-1) by real-time reverse transcription-polymerase chain reaction (RT-PCR) in rat colon tissues. This is in addition to oxidative stress markers in colon were performed across all groups. Results: The presence of aberrant crypt foci was reordered once histopathological examination of colon tissue from rats which received DMH alone. Administration of BMCs into rats starting from zero-day of DMH injection improved the histopathological picture which showed a clear improvement in mucosal layer, few inflammatory cells infiltration periglandular and in the lamina propria. Gene expression in rat colon tissue demonstrated that BMCs down-regulated survivin, β-catenin, MDR-1 and cytokeratin 20 genes expression in colon tissues after colon cancer induction. Amelioration of the colon status after administration of MSCs has been evidenced by a major reduction of lipid peroxidation, nitric oxide, and increasing of glutathione content and superoxide dismutase along with catalase activities. Conclusion: Our findings demonstrated that BMCs have tumor suppressive effects in DMH-induced colon cancer as evidenced by down-regulation of survivin, β-catenin, and MDR-1 genes and enhancing the antioxidant activity.

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Section: Discussionmentioning

confidence: 99%

Bone Marrow Cell Therapy on 1,2-Dimethylhydrazine (DMH)-Induced Colon Cancer in Rats

El‐Khadragy

Nabil

Hassan

et al. 2018

Cell Physiol Biochem

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“…S. neglecta alga was previously reported for its antioxidant, anti-bacterial and anti-inflammatory properties [ 22 , 23 , 36 , 37 ]. Regarding anti-cancer properties, S. neglecta water extract demonstrated in vivo cancer chemopreventive effects on DEN-induced hepatocarcinogenesis [ 25 ] as well as on the management of early stages of colon carcinogenesis in rat models [ 26 ]. In our previous study, using the plant-based metabolomic profiling technique, the S. neglecta ethyl acetate fraction inhibited PC3 prostate cancer cell metastasis via the inhibition of Akt/MAPK signaling pathway [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

“…For instance, the water extract of S. neglecta showed a protective effect against diethylnitrosamine-induced hepatocarcinogenesis in rats [ 25 ]. S. neglecta extract also inhibited the early stages of DMH-induced colon carcinogenesis in rats by modulating xenobiotic metabolizing enzymes, inhibition of cell proliferation, and induction of apoptosis [ 26 ]. In our previous study, we found that the ethyl acetate fraction of S. neglecta inhibited the metastasis of PC3 prostate cancer cells by inhibiting MMP-9 secretion, epithelial-mesenchymal transition, and the Akt signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

Pyrogallol from Spirogyra neglecta Inhibits Proliferation and Promotes Apoptosis in Castration-Resistant Prostate Cancer Cells via Modulating Akt/GSK-3β/β-catenin Signaling Pathway

Arjsri

Mapoung

Semmarath

et al. 2023

IJMS

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Castration-resistant prostate cancer (CRPC) is an advanced form of prostate cancer associated with poor survival rates. The high proliferation and metastasis rates have made CRPC one of the most challenging types of cancer for medical practitioners and researchers. In this study, the anti-cancer properties and inhibition of CRPC progression by S. neglecta extract and its active constituents were determined using two CRPC cell lines, DU145 and PC3. The ethyl acetate fraction of S. neglecta (SnEA) was obtained using a solvent-partitioned extraction technique. The active constituents of SnEA were then determined using the HPLC technique, which showed that SnEA mainly contained syringic acid, pyrogallol, and p-coumaric acid phenolic compounds. After the determination of cytotoxic properties using the SRB assay, it was found that pyrogallol, but not the other two major compounds of SnEA, displayed promising anti-cancer properties in both CRPC cell lines. SnEA and pyrogallol were then further investigated for their anti-proliferation and apoptotic induction properties using propidium iodide and Annexin V staining. The results showed that SnEA and pyrogallol inhibited both DU145 and PC3 cell proliferation by inducing cell cycle arrest in the G0/G1 phase and significantly decreased the expression of cell cycle regulator proteins (cyclin D1, cyclin E1, CDK-2, and CDK-4, p < 0.001). SnEA and pyrogallol treatments also promoted apoptosis in both types of CRPC cells through significantly downregulating anti-apoptotic proteins (survivin, Bcl-2, and Bcl-xl, p < 0.001) and upregulating apoptotic proteins (cleaved-caspase-9, cleaved-caspase-3 and cleaved-PARP-1, p < 0.001). Mechanistic study demonstrated that SnEA and pyrogallol inactivated the Akt signaling pathway leading to enhancement of the active form of GSK-3β in CRPC cell lines. Therefore, the phosphorylation of β-catenin was increased, which caused degradation of the protein, resulting in a downregulation of β-catenin (unphosphorylated form) transcriptional factor activity. The current results reflect the potential impact of S. neglecta extract and pyrogallol on the management of castration-resistant prostate cancer.

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Effect of Spirogyra neglecta on the early stages of 1, 2-dimethylhydrazine-induced colon carcinogenesis in rats

Cited by 2 publications

References 40 publications

Bone Marrow Cell Therapy on 1,2-Dimethylhydrazine (DMH)-Induced Colon Cancer in Rats

Bone Marrow Cell Therapy on 1,2-Dimethylhydrazine (DMH)-Induced Colon Cancer in Rats

Pyrogallol from Spirogyra neglecta Inhibits Proliferation and Promotes Apoptosis in Castration-Resistant Prostate Cancer Cells via Modulating Akt/GSK-3β/β-catenin Signaling Pathway

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