Antitumor and anti‐metastatic mechanisms of <i>Rhizoma paridis</i> saponins in Lewis mice

Man, Shuli; Chai, Hongyan; Cui, JingXia; Yao, Jingwen; Gao, Wenyuan

doi:10.1002/tox.22501

Cited by 19 publications

(15 citation statements)

References 27 publications

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“…Many cancer drugs can decrease MMP8 levels along with other MMPs: The plant-based isoflavones genistein and glycitein, as well as the flavone apigenin, down-regulate MMP8 expression in vitro and inhibit leukemia cell invasion [161,162] and decrease the viability of hepatocellular carcinoma cells [163]. Saponins from the plant Rhizoma paridis decreased the expression of inflammatory cytokines and MMP8 as well as reduced lung cancer tumor volume and growth in mice [164]. Therapeutic gold nanoparticles, which decreased ovarian cancer tumor growth and metastasis in vivo, also inhibited ovarian cancer cell proliferation, decreased MMP8 expression, and altered cytokine production in vitro [165].…”

Section: Resultsmentioning

confidence: 99%

The Role of MMP8 in Cancer: A Systematic Review

Juurikka

Butler

Salo

et al. 2019

IJMS

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Matrix metalloproteinases (MMPs) have traditionally been considered as tumor promoting enzymes as they degrade extracellular matrix components, thus increasing the invasion of cancer cells. It has become evident, however, that MMPs can also cleave and alter the function of various non-matrix bioactive molecules, leading to both tumor promoting and suppressive effects. We applied systematic review guidelines to study MMP8 in cancer including the use of MMP8 as a prognostic factor or as a target/anti-target in cancer treatment, and its molecular mechanisms. A total of 171 articles met the inclusion criteria. The collective evidence reveals that in breast, skin and oral tongue cancer, MMP8 inhibits cancer cell invasion and proliferation, and protects patients from metastasis via cleavage of non-structural substrates. Conversely, in liver and gastric cancers, high levels of MMP8 worsen the prognosis. Expression and genetic alterations of MMP8 can be used as a prognostic factor by examination of the tumor and serum/plasma. We conclude, that MMP8 has differing effects on cancers depending on their tissue of origin. The use of MMP8 as a prognostic factor alone, or with other factors, seems to have potential. The molecular mechanisms of MMP8 in cancer further emphasize its role as an important regulator of bioactive molecules.

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Section: Resultsmentioning

confidence: 99%

The Role of MMP8 in Cancer: A Systematic Review

Juurikka

Butler

Salo

et al. 2019

IJMS

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“…To further verify the bio‐function of TAMs exosomes in vivo, we constructed OS xenograft model by subcutaneous injection and metastases model as reported 22–24 . TAMs exosomes were injected through tail vein every 7 days (Figure 4A).…”

Section: Resultsmentioning

confidence: 99%

Tumor‐associated macrophages‐derived exo‐let‐7a promotes osteosarcoma metastasis via targeting C15orf41 in osteosarcoma

Yan

Xia

Qun

et al. 2023

Environmental Toxicology

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Background Osteosarcoma (OS) immune environment is complexed and the immune factors‐related to OS progression need to be explored. Tumor‐associated macrophages (TAMs) are regarded as immune suppressive and tumor‐promoting cells. However, the underlying mechanisms through which TAMs function are still fragmentary. Here, we aim to explore the underlying mechanisms by which TAMs regulate OS progression. Methods TAMs from OS tissues were isolated by flow cytometry. Exosomes derived from TAMs were separated using ultracentrifugation and western blotting. Transmission electron microscopy (TEM), and flow cytometry were constructed to characterize TAMs‐derived exosomes. Additionally, the differential MicroRNAs (miRNAs) and genes were detected through RNA sequencing, and further validated using real‐time PCR (RT‐PCR). OS cell metastasis ability was assessed using transwell invasion and scratch wound healing assays. MiRNAs mimic and lentiviral vectors were utilized to explore the effects on OS progression. Results Exosome secreted by TAMs accelerated the OS metastasis. Let‐7a level was upregulated in TAMs derived exosomes, which downregulated C15orf41 by targeting 3′‐untranslated region (UTR). Furthermore, overexpressing let‐7a enhanced invasion and migration by blocking the transcription of C15orf41. In consistent, up‐regulating let‐7a promoted OS progression and made the prognosis to be worse, which can be reversed by C15orf41 overexpression. Conclusion This study highlighted the critical role of TAMs‐derived exosomes in OS progression and explored the potential value of the let‐7a/C15orf41 axis as an indicator or target for OS.

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“…Rhizoma Paridis plays momentous roles in traditional Chinese medicine, and a large number of studies has confirmed that the main anticancer components of Rhizoma Paridis are steroidal saponins [ 21 , 22 ]. The steroidal saponins of Rhizoma Paridis have been demonstrated to induce cell cycle arrest, apoptotic cell death, and autophagy in human lung cancer cells [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Polyphyllin II Induces Protective Autophagy and Apoptosis via Inhibiting PI3K/AKT/mTOR and STAT3 Signaling in Colorectal Cancer Cells

Sun

Jiang

et al. 2022

IJMS

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Polyphyllin II (PPII) is a natural steroidal saponin occurring in Rhizoma Paridis. It has been demonstrated to exhibit anti-cancer activity against a variety of cancer cells. However, the anti-colorectal cancer (CRC) effects and mechanism of action of PPII are rarely reported. In the present study, we showed that PPII inhibited the proliferation of HCT116 and SW620 cells. Moreover, PPII induced G2/M-phase cell cycle arrest and apoptosis, as well as protective autophagy, in CRC cells. We found that PPII-induced autophagy was associated with the inhibition of PI3K/AKT/mTOR signaling. Western blotting results further revealed that PPII lowered the protein levels of phospho-Src (Tyr416), phospho-JAK2 (Tyr1007/1008), phospho-STAT3 (Tyr705), and STAT3-targeted molecules in CRC cells. The overactivation of STAT3 attenuated the cytotoxicity of PPII against HCT116 cells, indicating the involvement of STAT3 inhibition in the anti-CRC effects of PPII. PPII (0.5 mg/kg or 1 mg/kg, i.p. once every 3 days) suppressed HCT116 tumor growth in nude mice. In alignment with the in vitro results, PPII inhibited proliferation, induced apoptosis, and lowered the protein levels of phospho-STAT3, phospho-AKT, and phospho-mTOR in xenografts. These data suggest that PPII could be a potent therapeutic agent for the treatment of CRC.

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Antitumor and anti‐metastatic mechanisms of Rhizoma paridis saponins in Lewis mice

Cited by 19 publications

References 27 publications

The Role of MMP8 in Cancer: A Systematic Review

The Role of MMP8 in Cancer: A Systematic Review

Tumor‐associated macrophages‐derived exo‐let‐7a promotes osteosarcoma metastasis via targeting C15orf41 in osteosarcoma

Polyphyllin II Induces Protective Autophagy and Apoptosis via Inhibiting PI3K/AKT/mTOR and STAT3 Signaling in Colorectal Cancer Cells

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