Table 1 Role of PI3K/AKT pathway in squamous cell carcinoma of cervix

Metastatic or recurrent cervical SCC (n = 31)

–

–

–

–

–

Targeted PI3K/AKT/mTOR therapies in patients with heavily treated metastatic or recurrent cervical SCC who harbor PIK3CA mutation and/or PTEN loss/mutation are associated with a significant response rate and survival benefits

[6]

–

SiHa, ME-180, HeLa, C33A

DEPTOR siRNA

90 nM

Bcl-2,

Bcl-xL

PI3K/AKT,

p38 MAPK,

ERK1/2

DEPTOR silencing via down-regulating PI3K/AKT and by up-regulating p38 MAPK could induce apoptosis

[7]

–

SiHa, CaSki, C33A, MS751

FPS-ZM1

1 μM

RAGE, Bax,

Bcl-2, PCNA

PI3K/AKT

Downregulation of RAGE via modulation of PI3K/AKT can activate apoptosis and inhibit cell proliferation in cervical SCC

[8]

Primary cervical cancer (n = 70), normal cervical tissues (n = 30)

HeLa, SiHa,

ME-180, CaSki,

C-33A, C-4I, SW756, MS751

–

–

p27Kip1, AKT1

PI3K/AKT

Downregulation of p27(Kip1) could be regulated via the PI3K/AKT-mediated proteasomal degradation in CC cells

[9]

Primary CC (n = 35), normal cervical tissues (n = 35)

HeLa, CaSki, SiHa, ME-180, H8

–

–

ANRIL

PI3K/AKT

LncRNA ANRIL could promote carcinogenesis via PI3K/Akt pathway and can be considered as an indicator of poor prognosis

[10]

-

HeLa

Nicotine

0.1–10 μM

NF-κB

PI3K/AKT

Nicotine via induction of PI3k/AKT/NF-κB pathway promotes HeLa cell migration and invasiveness

[11]

Primary CC (n = 93)

Hela, Caski

LY294002,

cisplatin

10–30 nM, 10 μM

PAK4

PI3K/AKT

PAK4 via the PI3K/AKT pathway can contribute to the cisplatin resistance in CC cells

[12]

Primary CC (n = 136)

HeLa

–

–

PGRN,

TSC-2,

p70S6K

PI3K/AKT, mTOR, ERK

Growth factor progranulin (PGRN) via the PI3K/AKT/mTOR pathway can promote tumorigenesis of CC

[13]

Primary CC (n = 219)

HeLa, ME-180, SiHa, C33A, CaSKi, MS751

–

–

FOXC1

PI3K/AKT

FOXC1 via the PI3K-AKT signal pathway can promote proliferation and EMT in CC

[14]

Primary cervical cancer (n = 174), healthy volunteers (n = 30)

–

–

–

–

PI3K/AKT, mTOR

Exosome-mediated PI3k/Akt/mTOR pathway could be considered as a diagnostic biomarker in CC

[15]

–

SiHa, C33A, CaSki, HK-2,

WI-38, HeLa

Licochalcone A (LicA)

0–100 μM

LC3-II, Beclin-1,

Atg-5/7/12, Bcl-2, Caspase-3/9, JNK1/2

PI3K/AKT, mTOR

LicA via inactivating the PI3K/AKT/mTOR pathway could induce autophagy in CC cells

[16]

–

HeLa, SiHa, CaSki

–

–

S100A6, GSK-3β,

E-cadherin,

N-cadherin,

Vimentin, Snail, Twist

PI3K/AKT, mTOR

S100A6 via the PI3K/AKT pathway promotes proliferation and migration of CC cells

[17]

Primary CC (n = 72) healthy volunteers (n = 12)

CaSki

–

–

miR-433, FAK

PI3K/AKT

miR-433 via PI3K/AKT signaling by influencing expression of FAK could induce apoptosis in CC

[18]

Primary CC (n = 30) healthy volunteers (n = 12)

Hela, C33A,

SiHa, ME-180

–

–

miR-338, ATF2, LC3I/II, Bax,

Cyclin-D1, p27/35, Bcl-2, Caspase-3/9

PI3K/AKT, mTOR

miR-338 via the PI3K/AKT/mTOR pathway could modulate proliferation and autophagy in CC

[19]