Cannabinoids inhibit angiogenic capacities of endothelial cells via release of tissue inhibitor of matrix metalloproteinases-1 from lung cancer cells

Ramer, Robert; Fischer, Sascha; Haustein, Maria; Manda, Katrin; Hinz, Burkhard

doi:10.1016/j.bcp.2014.06.017

Cited by 59 publications

(69 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another potential anti-cancer activity of cannabinoids is related to their capacity to reduce cell migration, as observed in glioma [36], breast [7] and lung cancer [8], while no data was reported regarding MM. The homing of MM cells in bone marrow is associated with the progression of MM and patient's survival [37].…”

Section: Discussionmentioning

confidence: 99%

Cannabinoids synergize with carfilzomib, reducing multiple myeloma cells viability and migration

et al. 2016

View full text Add to dashboard Cite

Several studies showed a potential anti-tumor role for cannabinoids, by modulating cell signaling pathways involved in cancer cell proliferation, chemo-resistance and migration. Cannabidiol (CBD) was previously noted in multiple myeloma (MM), both alone and in synergy with the proteasome inhibitor bortezomib, to induce cell death. In other type of human cancers, the combination of CBD with Δ9-tetrahydrocannabinol (THC) was found to act synergistically with other chemotherapeutic drugs suggesting their use in combination therapy. In the current study, we evaluated the effects of THC alone and in combination with CBD in MM cell lines. We found that CBD and THC, mainly in combination, were able to reduce cell viability by inducing autophagic-dependent necrosis. Moreover, we showed that the CBD-THC combination was able to reduce MM cells migration by down-regulating expression of the chemokine receptor CXCR4 and of the CD147 plasma membrane glycoprotein. Furthermore, since the immuno-proteasome is considered a new target in MM and also since carfilzomib (CFZ) is a new promising immuno-proteasome inhibitor that creates irreversible adducts with the β5i subunit of immuno-proteasome, we evaluated the effect of CBD and THC in regulating the expression of the β5i subunit and their effect in combination with CFZ. Herein, we also found that the CBD and THC combination is able to reduce expression of the β5i subunit as well as to act in synergy with CFZ to increase MM cell death and inhibits cell migration. In summary, these results proved that this combination exerts strong anti-myeloma activities.

show abstract

Section: Discussionmentioning

confidence: 99%

Cannabinoids synergize with carfilzomib, reducing multiple myeloma cells viability and migration

et al. 2016

View full text Add to dashboard Cite

show abstract

“…TIMP‐1 belongs to family of TIMP gene and its proteins are natural inhibitors of the matrix metalloproteinase (MMPs), which is a group of peptidases involved in degradation of the extracellular matrix. It contributes to cell proliferation, participates in the most of the physiological and pathological processes involved in cell proliferation, migration, matrix remodeling, cell survival and matrix degradation …”

Section: Discussionmentioning

confidence: 99%

TUC.338 promotes invasion and metastasis in colorectal cancer

Wang

Zhou

et al. 2016

Int. J. Cancer

View full text Add to dashboard Cite

Ultraconserved regions (UCRs) are non-protein coding gene sequences that are strictly conserved across among different species. Emerging evidence demonstrates that transcribed ultraconserved regions (TUCRs) encoding noncoding RNAs serve as regulators of gene expression. In recent decades, increasing evidence implicates the involvement of UCRs in carcinogenesis. The role of TUC.338 in cervical cancers was an oncogene in previous studies. Until now, the role of TUC.338 in colorectal cancers remains undefined. This study revealed that TUC.338 is significantly up-regulated in colorectal cancers (CRC) tissue and CRC cell lines, and the up-regulated TUC.338 is associated with lymph node metastasis. Transfection with small interfering RNA (siRNA) markedly inhibited cell migration and invasion in SW480 and HCT116 colorectal cancer cell lines. TIMP-1 was demonstrated to be negatively regulated by TUC.338 at the posttranscriptional level, via a specific target site within the 3' untranslated region by dual-luciferase reporter assay. The expression of TIMP-1 was also observed to inversely correlate with TUC.338 expression in CRC tissues. Over-expression of TIMP-1 with migRI-TIMP-1-GFP inhibited CRC cell migration and invasion and down-regulates MMP9, resembling that of TUC.338-siRNA. Thus, these findings suggested that TUC.338 acts as a novel oncogene by targeting the TIMP-1 gene thus promoting colorectal cancer cell migration and invasion.

show abstract

“…TIMP1 is a member of the TIMP family, which are natural inhibitors of the MMPs, a group of peptidases involved in degradation of the extracellular matrix. TIMP1 participates in the majority of the physiological and pathological processes involved in cell proliferation, migration, matrix remodeling, cell survival and matrix degradation (14)(15)(16)(17)(18). It has also been reported that TIMP1 is overexpressed in colorectal and lung tumors (19,20), and is associated with metastasis and invasion in breast, upper urinary tract and oral squamous cell tumors (19)(20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

TUC338 promotes cell migration and invasion by targeting TIMP1 in cervical cancer

2017

View full text Add to dashboard Cite

Abstract. Ultraconserved regions (UCRs) are non-proteincoding gene sequences that are strictly conserved across numerous distinct species. It has been demonstrated previously that UCRs encoding non-coding RNAs serve as regulators of gene expression. In recent decades, there has been increasing evidence for the involvement of UCRs in carcinogenesis. In previous studies, the non-coding RNA transcribed ultraconserved element 338 (TUC338) was identified to serve an oncogenic role in hepatocellular cancer; however, thus far, the role of TUC338 in cervical cancer (CC) remains undefined. The results of the present study revealed that TUC338 is significantly upregulated in CC tissues and cell lines, and that the upregulation of TUC338 is associated with lymph node metastasis. Transfection with small interfering RNA (siRNA) against TUC338 could markedly inhibit cell migration and invasion in HeLa and C33A CC cell lines. Using a dual-luciferase reporter assay, tissue inhibitor of metalloproteinase 1 (TIMP1) was demonstrated to be negatively regulated by TUC338 at the post-transcriptional level, via a specific target site within the 3' untranslated region. The expression of TIMP1 was also observed to be inversely associated with TUC338 expression in CC tissues. Overexpression of TIMP1 with MigRI-TIMP1-green fluorescent protein inhibited CC cell migration and invasion and downregulated matrix metalloproteinase 9, resembling the effects of TUC338 siRNA. Therefore, the results of the present study suggest that TUC338 acts as a novel oncogene by targeting the TIMP1 gene, and inhibiting CC cell migration and invasion.

show abstract

Cannabinoids inhibit angiogenic capacities of endothelial cells via release of tissue inhibitor of matrix metalloproteinases-1 from lung cancer cells

Cited by 59 publications

References 53 publications

Cannabinoids synergize with carfilzomib, reducing multiple myeloma cells viability and migration

Cannabinoids synergize with carfilzomib, reducing multiple myeloma cells viability and migration

TUC.338 promotes invasion and metastasis in colorectal cancer

TUC338 promotes cell migration and invasion by targeting TIMP1 in cervical cancer

Contact Info

Product

Resources

About