Table 5.

Selenium containing compounds for cancer treatment

S.no	Name of the compounds	Structure	Types of cancer/cell lines	Dosage concentration in micromolar (µM)	Apoptosis mechanism	References
Inorganic selenium containing compounds
1	Sodiu m selenite		1) HSC-3, HSC-4, and SAS	5–100 µM for 2–5 days	Pronounced anti-proliferative effect of selenite against three oral cancer cell lines	Endo et al. (2017)
			2) Lung cancer cell lines (H157, H611, and U2020)	5 µM for 5 h	Played a role in natural killer (NK) cell-based anticancer immunotherapy where it could increase the susceptibility of cancer cells to CD94/NK group 2A-positive NK cells	Olm et al. (2009)
			3) HepG2, HeLa, and MCF-7 cells	–	Apoptosis of cancer cells occurs by accumulation in mitochondria which would subsequently damage mitochondrial function, structure and lead to cell death	Hu et al. (2018)
2	Sodium selenate		Human oral squamous carcinoma (KB) cells resistant to chemotherapeutic drug vincristine (KBV20C)	5, 10, 30, and 50 µM for 48 h	Produced a higher sensitizing effect on the KBV20C cells by arresting the cell cycle at G2-phase and activating apoptotic pathways	Choi et al. (2015)
Natural organoselenium compounds
3	Selenomethionine		1) Lung cancer cells -NCI-H460 and H1299	10–1000 μM	SeMet used in combination with ionizing radiation enhanced treatment	Yang et al. (2009)
			2) Mouse xenograft model of colorectal carcinoma (SW480)	10–1000 μM	Low systemic toxicity and high tumor selectivity has been reported	Shin et al. (2007)
			3) Colon cancer	100–1000 μM	Participation of decreased COX-2 expression	Baines et al. (2002)
			4) Breast and prostate cancer	10–1000 μM	Cell death is facilitated by caspases and ER stress	Suzuki et al. (2010a)
4	Selenocystine		1) Cervical cancer	100–1000 μM	Paraptotic-like mediated by ER stress and UPR	Wallenberg et al. (2014)
			2) Nasopharyngeal, Liver, Lung and Melanoma	1–20 μM	Cell death is facilitated by caspases, mitochondrial dysfunction/signalling and PARP cleavage	Poerschke and Moos (2011)
			3) Acute promyelocytic leukemia,	10–100 μM
			4) Colon cancer	1–100 μM
5	Methylseleno-cysteine		Breast cancer	100–1000 μM	Cell death is facilitated by caspases, ER stress, mitochondrial dysfunction/signalling and PARP cleavage	Suzuki et al. (2010b)
			Colon cancer	10–1000 μM
			Lung cancer	10–1000 μM
			Oral Squamous	10–1000 μM
6	Selenodiglutathione		Acute myeloid leukaemia	1–20 μM	Cell death is facilitated by ROS production and oxidative damage	Wallenberg et al. (2014); Tobe et al. (2015)
			Breast cancer	1–20 μM
			Cervical cancer	1–20 μM
			Lymphoma	1–20 μM
			Oral cancer	0.1–2 μM
Synthetic organoselenium compounds
7	Methylseleninic acid		Lung cancer	10–100 μM	Cell death is facilitated by caspases, ER stress, UPR, mitochondrial dysfunction/signalling and PARP cleavage	Poerschke and Moos (2011);Wang et al. (2014); Shigemi et al. (2017)
			Pancreatic cancer	0.1–2 μM
			Lymphoma	1–100 μM
8	Ebselen		Bone marrow cancer	10–100 μM	Cell death is mediated by mitochondrial signaling. Acts as a substrate for thioredoxin reductase and rapidly oxidizes thioredoxin, leading to oxidative stress	Zhang et al. (2014)
			myeloma
9	Ethaselen		Tongue cancer	1–20 μM	Cell death is mediated by thioredoxin reductase inhibition and subsequent oxidative stress	Xing et al. (2008); Wang et al. (2012)
			cervival, gastric, liver, lung cancers	0.1–2 μM
10	Diselenides		Colon cancer cells	1–100 μM	Cytotoxicity by cell-cycle arrest and caspase pathway	Nedel et al. (2012)
11	Selenazofurin		MCF-7 human breast carcinoma cells	0.1–2 μM	Pro-apoptotic activity and higher growth inhibition	Zhou et al. (2015)
			Bladder, cervical, colon, leukemia, lymphoma, kidney	0.1–2 μM in blood cell tumours, 1–20 μM in solid tumours	Act through non-competitive inhibition of inosine monophosphate dehydrogenase, thus limiting de novo guanine nucleotide biosynthesis	Franchetti et al. (1997)
12	Selenocyantes		CCRF-CEM, HT-29, HTB-54, PC-3 and, MCF-7 cell lines	1–100 μM	Increase in compound lipophilicity and thereby increasing the alkyl chain length was consistent In cells associated to a caspase-dependent apoptotic cell death through the induction of p53, Bax and suppression of Bcl-2	Romano et al. (2015)
13	Selenoesters		Prostate, breast, lung and colon cancer cell lines	Below 0.1 μM	Acting as GSH depleting agents	Dominguez-Alvarez et al. (2014)
			Human hepatoma cells		Ability to act as strong inhibitor of cellular efflux pump P-gp
			In mouse MDR T-lymphoma cells and in human colon cancer cells
14	Se-NSAID		Breast, colorectal, melanoma and pancreatic cancers	1–100 μM	Apoptosis mediated by caspases, PARP cleavage and ROS production. Involvement of COX-2 and PI3K/AKT inhibition	Gowda et al. (2013); Plano et al. (2016)
15	Selenoureas		Colon cancer cell models	Below 10 μM	Activation of caspase-dependent pathways and inhibition of antiapoptotic proteins	Alcolea et al. (2016)
16	Selenocarbonyl derivatives		MCF-7 cells	1–100 μM	Arresting the cell cycle and caspase pathway	Martins et al. (2015)

Dosage concentration (in vitro dose for 48–72 h IC₅₀)—very low (0.1–2 μM), low (1–20 μM), low to medium (1–100 μM), medium (10–100 μM), medium to high (10–1000 μM, high (100–1000 μM)