Outstandingly, let-7c behaves in an unusual manner than the common miRNAs by
binding to 3′UTR of Numbl and evidently increasing the expression of Numbl, an
inhibitor of Notch signalling (Miele et al. 2006). As a fact, tumour progression and
apoptosis were observed in these pancreatic ductal adenocarcinoma cells. The
influence of quercetin was also studied using in vitro oral cancer cells (HSC-6 and
SCC-9). Cells treated with quercetin expressed higher miR-16 expression which
was then shown to mediate the inhibition of HOXA10 level (Zhao et al. 2019). An
earlier in vitro study revealed HOXA10 to be positively related to the outcome of
cancer cell proliferation on head and neck squamous cell carcinoma (Guo et al.
2018). Collectively, the activated expression of miR-16 acted as a tumour suppressor in oral cancer by interrupting HOXA10 (Zhao et al. 2019). Likewise,
quercetin mediating expression of distinct microRNA: miR-16, miR-217 and
miR-145 were discovered through many studies conducted in lung adenocarcinoma, osteosarcoma, and ovarian cancer cells, respectively (Sonoki et al. 2015;
Zhang et al. 2015; Zhou et al. 2015).
Sulforaphane (SFN) originates as an isothiocyanate derivative of cruciferous
plants such as cauliflower and broccoli known to be effective as anticancer agent
based on reputable in vivo studies (Zhang and Tang 2007). Importantly, SFN
treated non-small cell lung (H1299, 95C and 95D) cancer cells which disclosed a
suppression of miR-616, an oncomiR modulating GSK3b/b-catenin signalling
pathway commonly implicated in cancer invasiveness (Wang et al. 2017). In particular, the SFN targets the EGFR signalling which is associated with EMT (epithelial mesenchymal transition) of lung cancer. Studies, however, indicate EMT
largely influencing the progression of metastasis, chemoresistance and other types
of tumours (Xiao and He 2010). Another study uniformly related to EMT was
recorded in SFN-treated bladder cancer cells, (T24 and UMUC-3). Consequently,
expression of (miR-200c) was greatly enhanced where it inhibits mesenchymal
phenotype (vimentin) and upregulated epithelial phenotype (E-cadherin), thus
bringing the mechanism of EMT down to a halt (Huang et al. 2018). Combination
treatment of SFN and iberin in colorectal cancer cell lines (NCM460 and NCM356)
exhibited better potential via upregulation of miR-23b and downregulation of
oncomiR, miR-27b. The performance of these miRNAs is contributed to the
anti-invasive, anti-angiogenesis and anti-proliferation activities in cancer cells
(Slaby et al. 2013). Of the reasons why pancreatic cancer cells are resistant to
treatment is due to the loss of gap junction intercellular communication and connexin 43 expression. However, PANC-1 cells treated with SFN seem to restore
these features by making cell sensitive again to anticancer drugs. This is achieved
by reducing the expression of miR-30a-3p thus enhancing the expression of Cx43, a
protein associated with gap junction (Georgikou et al. 2020). In another study of
breast cancer (MCF-7, MDA-MB-231 and SK-BR-3) cell lines, the introduction of
SFN dramatically reduced the expression of miR-23, miR-92b, miR-381 which
eventually promoted cell cycle arrest and senescence in these cells (Lewinska et al.
2017).
Genistein is a natural soy isoflavone that has featured exceeding intensity as an
anticancer agent (Spagnuolo et al. 2015; Varinska et al. 2015). In MCF-7 and
4 The Role of Phytochemicals in Cancer Prevention and Cure
141
binding to 3′UTR of Numbl and evidently increasing the expression of Numbl, an
inhibitor of Notch signalling (Miele et al. 2006). As a fact, tumour progression and
apoptosis were observed in these pancreatic ductal adenocarcinoma cells. The
influence of quercetin was also studied using in vitro oral cancer cells (HSC-6 and
SCC-9). Cells treated with quercetin expressed higher miR-16 expression which
was then shown to mediate the inhibition of HOXA10 level (Zhao et al. 2019). An
earlier in vitro study revealed HOXA10 to be positively related to the outcome of
cancer cell proliferation on head and neck squamous cell carcinoma (Guo et al.
2018). Collectively, the activated expression of miR-16 acted as a tumour suppressor in oral cancer by interrupting HOXA10 (Zhao et al. 2019). Likewise,
quercetin mediating expression of distinct microRNA: miR-16, miR-217 and
miR-145 were discovered through many studies conducted in lung adenocarcinoma, osteosarcoma, and ovarian cancer cells, respectively (Sonoki et al. 2015;
Zhang et al. 2015; Zhou et al. 2015).
Sulforaphane (SFN) originates as an isothiocyanate derivative of cruciferous
plants such as cauliflower and broccoli known to be effective as anticancer agent
based on reputable in vivo studies (Zhang and Tang 2007). Importantly, SFN
treated non-small cell lung (H1299, 95C and 95D) cancer cells which disclosed a
suppression of miR-616, an oncomiR modulating GSK3b/b-catenin signalling
pathway commonly implicated in cancer invasiveness (Wang et al. 2017). In particular, the SFN targets the EGFR signalling which is associated with EMT (epithelial mesenchymal transition) of lung cancer. Studies, however, indicate EMT
largely influencing the progression of metastasis, chemoresistance and other types
of tumours (Xiao and He 2010). Another study uniformly related to EMT was
recorded in SFN-treated bladder cancer cells, (T24 and UMUC-3). Consequently,
expression of (miR-200c) was greatly enhanced where it inhibits mesenchymal
phenotype (vimentin) and upregulated epithelial phenotype (E-cadherin), thus
bringing the mechanism of EMT down to a halt (Huang et al. 2018). Combination
treatment of SFN and iberin in colorectal cancer cell lines (NCM460 and NCM356)
exhibited better potential via upregulation of miR-23b and downregulation of
oncomiR, miR-27b. The performance of these miRNAs is contributed to the
anti-invasive, anti-angiogenesis and anti-proliferation activities in cancer cells
(Slaby et al. 2013). Of the reasons why pancreatic cancer cells are resistant to
treatment is due to the loss of gap junction intercellular communication and connexin 43 expression. However, PANC-1 cells treated with SFN seem to restore
these features by making cell sensitive again to anticancer drugs. This is achieved
by reducing the expression of miR-30a-3p thus enhancing the expression of Cx43, a
protein associated with gap junction (Georgikou et al. 2020). In another study of
breast cancer (MCF-7, MDA-MB-231 and SK-BR-3) cell lines, the introduction of
SFN dramatically reduced the expression of miR-23, miR-92b, miR-381 which
eventually promoted cell cycle arrest and senescence in these cells (Lewinska et al.
2017).
Genistein is a natural soy isoflavone that has featured exceeding intensity as an
anticancer agent (Spagnuolo et al. 2015; Varinska et al. 2015). In MCF-7 and
4 The Role of Phytochemicals in Cancer Prevention and Cure
141