Table 1 The studies employing MNPs for gastric cancer treatment

Gold

30 nm

Well treatment effect on MFC tumor cell

Active

both

Mouse forestomach carcinoma cell

[100]

Zinc

200–700 nm

Increased apoptosis in AGS cell lines by enhancing pro-apoptotic/blocking anti-apoptotic proteins and arresting cell cycle

Passive

both

AGS gastric cancer cell

[106]

Gold

300-700 nm

Increased apoptosis

Passive

In vitro

AGS cells

[101]

Gold

50-80 nm

suppressed cell growth

Active

both

MKN7 and MKN74

[108]

Gold

100 nm

antitumor effects

Active

In vitro

AGS and L929

[109]

gold

151 nm

Detection of methylated RPRM DNA in patients with high sensitivity

Active

In vitro

KATO III

[110]

gold

128 nm

induces apoptosis

Active

In vitro

AGS, SNU-5, and SNU-16

[100]

gold

10–40 nm

enhanced cell apoptosis

Passive

In vitro

A549, HT29 and AGS

[111]

gold

50 nm

suppressed tumor growth

Active

both

NCI-N87

[112]

gold

20 to 30 nm

Cytotoxicity effect

Passive

In vitro

MKN45, AGS, and KATO III

[113]

gold

5–60 nm

induce apoptosis

Passive

In vitro

AGS

[114]

silver

76 nm

cytotoxic potential

Passive

In vitro

AGS

[103]

silver

22 nm

apoptosis induction o

Passive

In vitro

AGS

[104]

silver

5–50 nm

induce apoptosis

Passive

In vitro

AGS

[115]

silver

20–50 nm

scavenging of free radicals and iron chelating activity

Passive

In vitro

AGS

[116]

iron oxide

67.3 nm

Prevention of metastasis

Passive

both

SGC-7901

[117]

Lanthanide

670 nm

Passive

In vitro

MKN45 and HeLa

[118]

gold

10, 20 and 40 nm

decreased invasion activity

Passive

In vitro

SGC-7901

[119]

gold

45.97 ± 4.67 nm

destroyed cell spindle morphology, ruptured cell

562 membranes

Passive

both

MCG803

[120]