Table 1 Represents the experimental TQ studies on CRC in vitro and in vivo

In vitro

HCT-116; 12 h: 60 µM

G1/S cell cycle arrest, enhanced apoptosis, increased p53 and p21,

decreased proliferation, reduced Bcl-2

[146]

HCT-116; 24 h: 35 µM

HCT-116; 48 h: 22 µM

In vitro

HT-29; 24 h: 51.6 ± 3.0 µM

HT-29; 48 h: 53.3 ± 1.7 µM

HT-29; 72 h: 51 ± 0.7 µM

Enhanced necrosis, decreased proliferation

[148]

In vitro and In vivo

C26; 24 h: 40 μM

Female Balb/c mice

Enhanced apoptosis and decreased ACF (not proliferation) in vivo, decreased invasion in vitro

[150]

In vitro

HCT-116; 24/48 h: 30/14 μM

LoVo; 24/48 h: 38/28 μM

DLD-1; 24/48 h: 42/23 μM

Caco-2; 24/48: 15/12.5 μM

HT-29; 48 h:110 μM

FHs74Int (Normal Cell Line)

Enhanced apoptosis (caspase-3) in DLD-1 (not HT-29), increased ROS in DLD-1 and Caco-2, decreased proliferation of all CRC cell lines (not FHs74Int)

[126]

In vitro and In vivo

DLD1; 196 μM

HCT116; 118 μM

RKO; 86 μM

HCEC-1CT; 79 μM

HT29; 160 μM

LoVo; 36 μM

Apc^Min mice

Enhanced apoptosis in polyps, decreased proliferation (Ki-67) of villi, reduced c-myc expression in polyps and in vitro, RAS/RAF/MEK1/2 inhibition, Wnt/ β-catenin inhibition, suppressed GSK-3β phosphorylation

[143]

In vitro

HCT-116

Enhanced apoptosis (increased p21, p27, cleavage of caspases-3/7/9 and PARP), decreased activated form, JAK2/STAT3 inhibition, Src inhibition

[145]

In vitro

HCT-116; 72 h: GI50: 12.7 ± 0.9 μM

HT-29; 72 h: GI50: 27.3 ± 3.0 μM

Enhanced apoptosis (mainly through late apoptotic process), increased NQO1 protein level, decreased (glutathione) GSH activity

[147]

In vitro

HCT-116; 24 h: 64.15 ± 2.80 µM

Enhanced apoptosis (increased caspase-3 activity/mRNA levels and Bax while decreased Bcl-2) in combination with Doxorubicin

[158]

In vitro and In vivo

HCT-116; 59.64 μM

Immunodeficient female NCr nude homozygous mice

Free TQ and TQ-NP decreased tumor volume/weight alone or with Doxorubicin

[136]

In vitro

HT-29

Increased mRNA/protein levels of PPAR-γ

[159]

In vitro & In vivo

HCT-116; 48/72 h: 40 µM

HCT-116/5FU; 48 h: 60 µM

NOD-SCID mice

Enhanced apoptosis (increased p53 and p21 while reduced NF-κB, PCNA and p-MEK protein levels), suppressed CD44, decreased migration/invasion of 5-FU sensitive and resistant cells

Decreased tumor growth (increased p53, p21, γ-H2AX, Iκβα, and reduced PCNA, NF-κB (p65), and p-MEK), suppressed CD44 in 5-FU sensitive xenograft mice

[160]

In vitro

Dox-treated HCT-116; 24 h: 66.75 ± 2.00 µM

Enhanced apoptosis

[161]

In vivo

Azoxymethane-induced CRC rats

Decreased ACF, Wnt, β-catenin, NF-κB and COX-2, while increased DKK-1 and CDKN1-A mRNA levels, decreased TGF-β1, COX-2, HSP-90 and VEGF protein levels

[133]

In vitro and In vivo

LoVo

Nude mice

Inhibited migration, decreased p-PI3K, p-Akt, p-GSK3β, β-catenin, COX-2, and LEF-1/TCF-4 in vitro, Decreased COX-2, β-catenin, and p-Akt in vivo

[141]

In vitro

COLO205

HCT116

Increased chemosensitivity to cisplatin, Suppressed NF-κB p65 phosphorylation, VEGF, c-Myc, and Bcl-2 protein levels,

[129]

In vivo

AOM-induced CRC rate

Increased DKK-1, CDNK-1A, TGF-β1, and Smad4, suppressed Wnt, β-catenin, NF-κB, and COX-2 mRNA levels

[162]

In vitro

HT-29; 24 h: 59.2 µM

HT-29; 48 h: 68.4 µM

Enhanced apoptosis, decreased proliferation

[163]

In vitro

CPT-11-R LoVo; 24 h: 6–8 µM

Increased unphosphorylated BAD, and reduced phosphorylated BAD

increased autophagic cell death (upregulated Atg5, Atg7, Atg12, Beclin-1, LAMP2, LC3-II, and SQSTM1/p62, while downregulated Atg3), decreased IKKα/β and NF-κB, suppressed EMT and metastasis (decreased Snail, Twist, vimentin, MMP-2/9), inhibited ERK1/2 and PI3K, enhanced JNK and p38

[164, 165]

In vitro

HCT-116; 24 h: 21.71 µM

HCT-116; 48 h: 20.53 µM

SW480; 24 h: 10.26 µM

SW480; 48 h: 10.50 µM

Decreased colony formation, proliferation, EMT, migration and invasion Reduced glucose fermentation, lactate production, and ATP production, Suppressed HexoKinase 2, PI3K/Akt, E-cadherin, increased N-cadherin

[139]

In vitro

HT29

SW480

SW620

Enhanced apoptosis, p21, p27, PTEN, BAX, Cytochrome-C, Caspase-3

Reduced proliferation, CCND1, CCND3, BCL-2, suppressed PI3K/AKT/mTOR

[140]

In vitro

HT29

SW480

SW620

Enhanced G2/M cell cycle arrest apoptosis, reduced CCND1, CCND3, PCNA, survivin, HIF1α, LDHA, and PDHK1, inhibited PI3K/AKT/mTOR, RAPTOR, and RICTOR, augmented p21, p27, BAX, Cytochrome-C, cleaved Caspase-3, PTEN, AMPKα, and PDH, increased ROS/RNS, MDA, and PCC, while reduced total GSH and catalase (CAT)

[61]

In vitro

HCT-15; 24 h: 82.59 μM

Reduced proliferation, Bcl-2, and miR-21-5p expression

[130]